6. Localization of UMN & Cortical Lesions.pdf

*I’ve Used Batch 17 + all in one Dr. Amr A. Qoora Consultant IM &Neurology Mubarak Al-Kabeer Hospital 26-09-2022 The doctor was basically reading the slides , but I included any additional information and batch 18’s tafreegh Dalal Alfayyadh This case wasn’t included b his slides • A 72-year-old...

*I’ve Used Batch 17 + all in one Dr. Amr A. Qoora Consultant IM &Neurology Mubarak Al-Kabeer Hospital 26-09-2022 The doctor was basically reading the slides , but I included any additional information and batch 18’s tafreegh Dalal Alfayyadh This case wasn’t included b his slides • A 72-year-old woman with a history of diabetes and hypertension suddenly awakens with deviation of her mouth angle to the left, weakness of the right arm and leg. On examination, she has upper motor neuron weakness of the right face, arm and leg associated with brisk reflexes on the right and a right extensor plantar response. } } The upper motor neuron is formed of the cortical motor neurones (the precentral gyrus), the motor pathways in the brain that (pass through the internal capsule), motor pathways in the brain stem (where decussation of tracts on to the contralateral side take place) to meet the cranial nerves of the contralateral side. This crossing takes place in the pyramidal decussation, where the anterior corticospinal tract (non crossed) is separated from the pyramidal tract (being the crossed part of the motor pathway). WHAT AN UPPER MOTOR NEURON FUNCTION Upper motor neuron control lower motor neuron through two different pathways • Pyramidal tract • Extra pyramidal tract 2 pathways 1- pyramidal tract e.g. corticospinal tract 2- extra pyramidal tract e.g. reticulospinal , vestibulospinal , tectospinal tracts PYRAMIDAL TRACTS •corticospinal tract EXTRAPYRAMIDAL TRACTS•Reticulospinal •Vestibulospinal •Tectospinal •Rubrospinal tract •Corticobulbar tract •Corticorubral tract } } Largest descending pathway in man Commonly referred to as pyramidal tract Lower motor neurone after decussation Before crossing >> contralateral After crossing >> ipsilateral dexterity refers to an inability to coordinate muscle activity in the performance of a motor task } AKA SPASTIC PARALYSIS AKA SUPRANUCLEAR PARALYSIS 1. Initially there is loss of tone in the affected muscles Shock stage, instead of being hypertonic, the patient will be hypotonic with flaccid muscles 2. Soon after the muscles gradually become resistant to passive some time the muscle gradually will change from movement and yield SPASTIC PARALYSIS. After hypotonia to spasticity, so hypertonia will occur( in few days to a week) 3. The myotatic deep tendon reflexes are increased in force and amplitude known as HYPERREFLEXIA. 4. The SUPERFICIAL REFLEXES are lost or diminished. Diminished then will be lost completely, like abdominal reflexes + cremastic reflexes 5. Positive Babinski’s Sign is noted. Big toe will go up And fanning of the other toes 6. If the suspected lesion is above the pyramidal decussation, the symptoms will be found on the contralateral side. 7. If the suspected lesion is below the pyramidal decussation, the symptoms will be found on the ipsilateral side. Lesion above the decussation >> contralateral symptoms Lesion below the decussation >> ipsilateral symptoms UPPER MOTOR NEURON LESIONS SIGNS & SYMPTOMS PYRAMIDAL TRACT + EXTRAPYRAMIDAL TRACTS -SPASTIC PARALYSIS ( Hemiplegia or Hemiparesis ); SPASTICITY = Increased resistance to passive movement Hemiplegia= complete paralysis Hemiparesis= partial paralysis - Muscular Weakness on paretic side - Loss of speed and agility on paretic side - Complete loss of control over distal muscles (Intrinsic muscles of hand) -Abnormal Reflexes Like ankle - Increased DTR’s ( Hyperreflexia) colnus which usually will - Clonus ( Series of rhythmic alternating contractions of agonist and not be present antagonist muscles ( Lowered threshold for DTR’s) in acute settings bc it - Clasp-Knife Reflex (Increased resistance to stretch followed by takes at least loss of resistance ( Lowered threshold for DTR’s and Golgi Tendon 10 days to develop and Reflexes spasticity takes few - Babinski Sign ( Dorsiflexion of big toe, fanning of little toes after days up to one or two weeks stroking sole of foot). to develop Note: Lesions restricted to the Corticospinal Tract alone , e.g., M1 Cortex, may NOT exhibit spasticity Clasp-knife reflex is like the clasp knife with initial spasticity or initial resistance to movement and then the resistance will be released SPASTICITY & ASSOCIATED HYPERTONIA Lower limb Upper limb UPPER MOTOR NEURON LESIONS UMNL LL= spastic on extension UL= spastic on flexion LOWER EXTREMITY Extensor Hypertonia w/stiff spastic gait & Circumduction at Hip joint UPPER EXTREMITY When try to examine the patient passively for the movement around a joint there will be great resistance related to speed, meaning when the examiner increases the rapidity of manipulation the resistance will increase, then it will be released suddenly bcz it is involving usually one group SPASTICITY of muscles, the lower limb is usually the extensors and the upper limb is flexors so involve either agonist or antagonist group Flexor Hypertonia w/loss of Intrinsic muscles of hand (skilled movement). Grasping movement of hand is spared = Increased resistance to passive movement . More rapid the manipulation, the greater the resistance. This is quickly followed by the collapse of resistance ( Clasp – Knife Phenomenon ) UPPER MOTOR NEURON LESIONS Patellar (DTR) Reflex Patellar (DTR) UMNL Normal Hyperreflexia I When striking the quadriceps tendon in the knee by the hammer it will contract, so the leg will extend and the quadriceps muscle will contract, so normal when the extension is small Exaggerated reflex According to google, striking the patellar tendon causes the quadriceps muscle to contract. INCREASED DTRs = Greater or brisker reflex response PLANTAR REFLEX (Nociceptive) UPPER MOTOR NEURON LESIONS Perception of pain NORMAL RESPONSE – Plantar flexion of all toes Babiniski sign, strike the lateral side of the sole of the foot with increasing the strike until reaching the base of big toe using blunt object not sharp, if normal there will be flexion of the toes so the big toe will go down with the other toes, but abnormal when extension of the great toe with fanning of Positive Babinski sign the other toes happen, so the big toe goes up and other toes separate in fan pattern Stroke sole of foot firmly in direction of arrows Extension or BABINSKI SIGN – Dorsiflexion of big toe, fanning of little toes (Seen in Pyramidal – Lateral Corticospinal Tract lesions) Babinski sign is normal in newborn bcz the corticospinal pathways (bundles of nerve bers) running from the brain and down the spinal cord are not fully myelinated (sheathed) in newborns and infants. Positive Babinski sign The cremasteric re ex is a super cial re ex found in human males that is elicited when the inner part of the thigh is stroked. UMN LESION } LMN LESION Paralysis affect movement rather than muscles } Muscle wasting is only from disuse, therefore slight. Occasionally marked in chronic severe lesions. } More localized Affect a group of muscles } Individual muscle or group of muscles are affected. Wasting pronounced. Initially from the beginning there is muscle wasting Usually no muscle wasting except from the disuse if the patient is not using the muscle } Spasticity of claspknife’ type. Muscles hypertonic. } Flaccidity. Muscles hypotonic. Normal or hypotonic } } Tendon reflexes increased. Clonus often present. Superficial reflexes diminished or modified. Abdominal reflex absent. Babinski’s sign +ve, Increased jaw jerk. } } Tendon reflexes diminished or absent. Superficial reflexes often unaltered. If I have a patient w/ facial palsy > I have to look if 1. The weakness involve upper & lower face > LMNL 2. Weakness involved only the lower face > UMNL .If the weakness involved upper & lower face >> LMNL . If the weakness involved only lower face >> UMNL • Step 1: Is it UMN or LMN? • Step 2: If UMN: 1. Brain (including brainstem). 2. Spinal cord. Characteristics of internal capsule lesion: } 1- Hemi-plegia i.e. paralysis of the muscles present in the opposite side of the body due to damage of pyramidal and extra- pyramidal tracts fibers. } 2- Hemi-anesthesia i.e. loss of all sensations from the opposite side of the body due to damage of sensory radiation. Above decussation > opposite side If optic radiation is involved } } 3- Hemi-anopia i.e. loss of vision in the opposite halves of visual fields of both eyes. So, lesion in the right internal capsule leads to loss of vision in the left halves of visual fields of both eyes. It is due to damage of optic radiation. 4- Decrease hearing; it is due to damage of auditory radiation. No deafness because each ear is bilaterally represented in the cerebral cortex. Midbrain 3 4 Pons 56 78 Medulla 9 10 11 12 Brain stem lesion } produces crossed hemiplegia i.e cranial nerve is affected on one side and the hemiplegia of the opposite side } If 3rd nerve is involved. Lesion is in midbrain } If 6th and 7th nerve is involved,lesion is in pons. } If 9th and 10th nerves are involved, lesion is in medulla Example: if I have right side UMNL in the brainstem >> right sided facial n. & left sided body affected @ the same side of the lesion PSEUDOBULBAR PALSY results from an upper motor neuron lesion to the corticobulbar pathways in the pyramidal tract. • It results from bilateral lesion of UMN’s of the muscles of the tongue (XII), face (VII), speech and swallowing (IX,X) • Individuals with pseudobulbar palsy also demonstrate inappropriate emotional outbursts. Bulbar palsy= weakness of balance, usually LMNL Pseudobulbar palsy= UMNL In brainstem not the cortex Spinal cord Whenever there is a lesion of spinal cord ,there will be UMN signs below the level of lesion } Upper limb involved ---- above C 5 } Absent abdominal reflexes----- above T 8 } Specific sensory level is always present After decussation Lesion should be If below T8 >> abdominal re exes are present Lesion should be Loss of sensation from the foot to the lvl of the lesion e.g. lesion b T10 >> loss sensation men the foot le lvl T10 } Depends upon hemispheric dominance } Non-neurologists generalize: If it’s left or right Most ppl left side ◦ right: visual/spatial, perception and memory ◦ left: language and language dependent memory } Look for aphasias, apraxias, and agnosias Impairment of language Loss of mental control of previously learned fine movement Ex: pt who can brush his teeth can’t do it now although he has good vision & hearing Unable to recognize persons, objects In spite of knowing them before, however, he can recognise his voice ( visual agnosia) } } } } } } Higher Cortical Function: you may see an aphasia, apraxia, or an agnosia Cranial Nerves should be normal, unless there is forced eye deviation Cerebellar function should be normal Motor exam may reveal weakness of face/arm>leg (or vice versa) with hypertonia if corticospinal tracts are hit Sensory exam may be abnormal (face/arm>leg, or vice versa) Reflexes may be abnormal (hyper-reflexia), and Babinski’s reflex may be present if the corticospinal tracts are hit Bc problem in the cortex More than UMNL Right visual cortex will cause left visual ... PLAY } Focal: depends on location of lesion ◦ motor or sensory loss from contralateral motor or sensory cortex ◦ aphasia from peri-Sylvian lesions in the dominant hemisphere ◦ ‘silent’ areas such as the anterior frontal lobes do not produce neurological signs if got a focal lesion, may have ◦ lesions of the cortex can become epileptic foci So contralateral seizure Disconnection of the cortex from the NS Generalized: decorticate state – destruction of cortex or disconnection from rest of nerv. system (white matter disease) } Total bilateral destruction : coma (although reticular formation destruction is a more common cause of coma) } Partial cortical destruction : acute: delerium; chronic: dementia } Decorticate posturing is described as abnormal exion of the arms with the extension of the legs Visual Fields: The presence of a homonymous hemianopia implies a lesion of the optic radiation of occipital cortex: if acute, this suggests a vascular lesion, typically an infarction of the middle cerebral artery territory. Left homonymous hemianopia due to right occipital lesion Can’t see the temporal eld Can’t see the right side of each eye If you have bilateral occipital lesion, you will have bilateral visual loss(cortical blindness) with macular sparing Cortical Functions - Language Happened only in cortical lesions ( bel dominant side which is the left side in most ppl) § Aphasia/dysphasia – true language disturbance with errors of grammar, word production and / or comprehension This should be differentiated from disorders of speech production: Eg Problems in the tongue, pharynx, or mouth or generalized trauma § Dysarthria – disorder of articulation due to the motor function underlying speech in which language is intact § Dysphonia – impairment of the ability to produce sounds due to disorder of larynx or its innervation § Aphonia – total loss of voice often due to bilateral recurrent laryngeal nerve injury, resection of larynx, etc. Cerebral Dominance / Lateralization § 90% of the population is definitely right-handed q 99% of these are strongly left hemisphere dominant for language § The 10% who are left-handed are different: q 80% have some degree of language representation in both hemispheres Language testing § Handedness Ask the patient if he is right or left handed § Spontaneous speech: fluency, articulation, prosody, grammar, errors (paraphasia's) § Comprehension: single words, yes/no questions, complex commands § Repetition Very imp, Give him a sentence and ask him to repeat § Naming Give him an object and ask him to name it § Reading/ Writing Give him a newspaper and ask him to write a paragraph Broca’s aphasia § § § § Lesion in dominant inferior frontal gyrus Non fluent aphasia Comprehension good Associated contralateral hemiparesis if nearby motor strip is involved http://www.google.com/imgres?imgurl=http://www-rohan.sdsu.edu/~ He understands you but can’t express what he wants= word finding difficulty Understand well Pt is fluent but non comprehensive, can’t understand very well Repetition is impaired } } } } Is characterized by fluent but meaningless speech output and repetition, with poor word and sentence comprehension. Meaningless speech, fluent and non-laboured Does not strain to produce words and does not appear to be searching for them It is typically due to ischemia in the posterior superior temporal cortex, in the distribution of the inferior division of the left MCA. } } } } Conduction aphasia is characterised by disproportionately impaired repetition with otherwise fluent speech. It is typically due to ischaemia affecting the inferior parietal lobule. Transcortical aphasia is characterised by relatively spared repetition. Transcortical sensory aphasia usually results from ischaemia involving the watershed area between the left MCA and left posterior cerebral artery (PCA) territory. Transcortical motor aphasia usually results from ischaemia involving the watershed area between the left MCA and left anterior cerebral artery (ACA) territory. Involves both areas ( Broca’s and Wernickle’s area) } Global aphasia denotes severe impairment in all aspects of language; the area of ischaemia often involves both anterior and posterior language areas (Broca and Wernicke areas). ◦Cortical sensory loss: }Graphesthesia }Sterognosis }Double Simultaneous Stimulation (2-point discrimination ) }Intact primary sensation with deficits in cortical sensation such as agraphesthesia or astereognosis suggests a lesion in the contralateral sensory cortex. Note, however, that severe cortical lesions can cause deficits in primary sensation as well. Extinction with intact primary sensation is a form of hemineglect that is most commonly associated with lesions of the right parietal lobe. Extinction can also be seen in right frontal or subcortical lesions, or sometimes in left hemisphere lesions causing mild right hemineglect Cortical sensations Ask the patient to close his eyes, then using 2 pins touch his hand, the distance between the 2 pins should be 2 mm, it is abnormal test if he can’t feel more than 5 mm, and he should know if the examiner is pricking him with one or two objects Ask the patient to close his eyes then put a familiar object on his hand, then ask him what is the object, and he should know by touching it Then test the other hand using different object Ask the patient to close his eyes and draw a number on his palm then ask him what is the number, if he can’t recognize then the opposite parietal lobe is injured } } } } Frontal Lobe Responsible for movement, judgment, personality, language Primary motor cortex: planned control of fine movements Prefrontal cortex: decision making Frontal lobe damage may cause: Frontal lobe lesion= No motor weakness } • personality and behaviour changes, e.g. apathy or disinhibition } • loss of emotional responsiveness or emotional lability } • cognitive impairments, e.g. memory, attention and concentration } • dysphasia (dominant hemisphere) } • conjugate gaze deviation to the side of the lesion Opposite to brainstem lesion > deviation } • urinary incontinence away from the lesion } • primitive reflexes, e.g. grasp } • focal motor seizures (motor strip). } } } } Parietal Lobe Responsible for sensory processing (touch, pain, temperature, body parts in space) Primary somatosensory cortex Damage: no conscious perception of touch If one side of the parietal lobe is damaged, contralateral disturbance of sensation will happen, and it is called central sensory loss Parietal Lobe Syndromes Usually left side § Dominant hemisphere: q q Ask the patient to open his eyes, and if he has no facial weakness and he understands then he doesn’t have aphasia!! If he can’t do that then he has apraxia Apraxias – inability to carry out an action in response to verbal command in the absence of problems with comprehension, has good balance, vision, power, understand you very well & u impairment of motor function. Pt ask him to walk he can’t respond Gerstmann’s syndrome: impaired calculation, left-right confusion, finger agnosia, dysgraphia Can’t know his left side from right § Nondominant hemisphere: q q Neglect of opposite side Impaired constructional ability } } } } Temporal Lobe Responsible for auditory processing Hippocampus: memory Amygdala: emotions Temporal lobe dysfunction may cause: } • memory impairment } • focal seizures with psychic symptoms } • contralateral upper quadrantanopia } • receptive dysphasia (dominant hemisphere). Occipital Lobe } Responsible for vision. Damage may cause: -Visual field defects: hemianopia (loss of part of a visual field) or scotoma (blind spot) - Visual agnosia: the inability to recognise visual stimuli - Disturbances of visual perception, e.g. macropsia (seeing things larger) or micropsia (smaller) - Visual hallucinations. If both nerves are e ected Conjugate eye movement Deviate towards the lesion If the patient comes with fever and headache 1- with seizure >> most probably due to encephalitis 2-No seizure >> most probably due to meningitis Can’t talk the loss of ability to execute or carry out skilled movement and gestures, despite having the physical ability and desire to perform them Gerstmann syndrome is a neuropsychological disorder characterized by the tetrad of agraphia (inability to write), acalculia (inability to perform mathematical calculations), nger agnosia (inability to name, discriminate, or identify ngers), and leftright disorientation (inability to distinguish left from right). Wasn’t included b his slides Wasn’t included b his slides Wasn’t included too • A 72-year-old woman with a history of diabetes and hypertension suddenly awakens with deviation of her mouth angle to the left, weakness of the right arm and leg. On examination, she has upper motor neuron weakness of the right face, arm and leg associated with brisk reflexes on the right and a right extensor plantar response.