Localising the lesion: “where in the CNS”



Localising the lesion: “where in the CNS”Learning objectivesDefinition of CNS and PNSDefinition of UMN and LMNFunction of each of the cerebral lobesThe homunculusCircle of willis and blood supply to the cerebral hemispheresMotor tracts – lateral corticospinalSensory tracts – lateral spinothalamic and dorsal columnsStroke syndromesClinical case scenariosDefinitionsCNS = Brain and spinal cordPNS = anything outside brain and spinal cordAlso include autonomic nervous system and cranial nervesMotor control systemsCorticospinal (pyradmial)Skilled, intricate, strong and organised movementsDefectiveness loss of skilled voluntary movement, spasticity and reflex changes Such as hemiparesis, hemiplegia or paraparesisExtrapyradimal systemFast, fluid movements that the corticospinal system has generatedDefectiveness bradykinesia, rigidity, tremor, choreaSuch as huntingtonsThe cerebellumCo-ordinating smooth and learned movement initiated by the pyradimal system and in posture and balance controlDefectiveness ataxia, past pointing, action tremor and incoordinationThe motor systemPyradimal motor system are the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the?medulla. The?pyramidal pathways?the lateral and anterior corticospinal?tracts directly innervate motor neurons of the spinal cord or brainstem of the anterior horn cells. whereas the extrapyramidal system centers around the modulation and regulation of the pyradimal tracts via indirect control of anterior horn cells.Extrapyramidal tracts modulate motor activity without directly innervating motor neurons.The corticospinal systemThe homunculusUMN vs LMNUMNLMNWastingnoyesFasciculationnoyesToneincreaseddecreasedPowerdecreaseddecreasedReflexesincreaseddecreasedPlantarsup goingdown goingSensory pathwaysPeripheral nerves carry sensation from dorsal roots to the cordPosterior columns (dorsal columns)Vibration, joint position, light touch and point discriminationCross in the brainstem passing to the thalamusSpinothalamic tractsPain and temperatureCross within the cord and pass in the spinothalamic tracts to the thalamus and reticular formationSensory cortexFibres from the thalamus pass to the parietal region sensory cortex and motor cortexCortical functionsFrontal lobeReasoning, planning, parts of speech, movement, emotions and problem solvingLeft frontal = broccas area (aphasia)Parietal lobeMovement, orientation, recognition, perception of stimuliOccipital lobeVisual processingTemporal lobePerception and recognition of auditory stimuli, memory and speechLeft temporal = wernicke’s areaCerebellumBalance and co-ordinationBasal gangliaInitiation and inhibition of movementWernickes area – like broccas area is it the understanding of written and spoken speechCircle of WillisInternal carotid artery supplies brainExternal carotid artery supplies faceMiddle cerebral artery supplies 1/3rd of brainVertebral arteries join to form the basillar artery which join at the base of the brainStrokeTACS – All three ofHemiplegia or hemi sensory lossVisual field defectDisturbance of higher functionDysphasiaDysphagiaPACS – 2 out of 3LACS – blockage of small branch of big arteryNo visual field defectPure motor strokePure sensorySensory motorAtaxiaPOCS – brain stem, cerebellum, cranial nervesBilateral motor or sensoryConjugate eye movement disorderCerebeller dysfunctionHemiplegia or cortical blindnessAcute occlusion of blood vessel leading to hypoxia and infarctionRisk factors DM, hypertension, smoking, hypercholesterolemia, FHx, AFInvestigations bloods, CT, MRI, carotid dopplers, Echo, ECG, 24 hour tapeTreatment in ischaemic strokeAspirinClopidogrelSupportive managementIn ischaemic stroke you have in ischaemic penumbra which is the area of the brain which is damaged during ischaemia in order to reduce the effects from this you need to optimise conditions – temp, BP, glucoseCerebellar syndromeCausesVascular lesionAlcoholDemyelinationTumoursHypothyroidismMetabolic disordersSigns “DANISH”DysdiadochokinesisAtaxiaNystagmusIntention tremorSlurred speech, dysarthriaHpyotonia, hyporeflexiaMultiple SclerosisAreas of demyelination and perivascular inflammation (white plaques)Disseminated in time and occurring anywhere within CNSAetiology - ?autoimmune ?vitamin D deficiencyClassificationBenign -little disease activity for many years, minimal disabilityRelapse remitting - most common, repeated attacks with periods of recoverySecondary chronic progressive - continuous progression of symptoms following an initial relapsing and remitting disease coursePrimary progressive - accumulation of pernament disability over time with superimposed relapsesInvestigationsLP – increased protein, increased immunoglobulin, oligoclonal bandsVisual evoked potentialsMRIOn examinationUnsteady gaitReduced proprioceptionBrisk reflexesBrown-sequard syndromeLoss of movement on same side as damageLoss of pain and temp and sensation on opposite sidespinal cord lesion where there is an incomplete lesion characterized by loss of motor function loss of vibration sense and fine touch, loss of?proprioception ?and signs of weakness on the same side of the spinal injury. This is a result of a lesion affecting the?dorsal column and the?corticospinal tract. On the contralateral side of the lesion, there will be a loss of pain and temperature sensation and crude touch 1 or 2 segments below the level of the lesionManagementSymptoms control (tremors, pain, muscle spasms)Steroids - severe relapses to speed up any recovery with will occur naturally. A severe relapse is usually classed as one that has significantly affected activities of daily livingBeta-inferons and Glatiramer - reduce rates of relapses by 30% and is only used in relapsing and remitting or relapsing progressive diseaseIV natalizumab - is a newer monoclocal antibody treatment used in patients with very severe active disease that can reduce relapses by 80%, cost, practical consideration and complications limits its use.Motor neurone diseaseDegeneration of upper and lower motor neurones of unknown cause5-10% autosomal dominantTypesSpinal muscular atrophy – limb weakness due to involvement of spinal cord anterior horn cellsPrimary later sclerosis – spastic limb weakness due to UMN involvement of the spinal cordProgressive bulbar palsy – involvement of bulbar motor neurones, progressive diseaseAmyotrophic lateral sclerosis – mixture of all the aboveInvestigationsDiagnosed clinically after other causes excludedEMG confirms fasciculation's and fibrillationsManagement – symptom controlFatal within 3-5 yearsCardiac and smooth muscle aren’t involved and ocular muscle very rarelyAutonomic dysfunction occurs lateSignsDysarthria, brisk jaw reflexFasciculation/wasting in deltoids, biceps, quadriceps and in tongueWeakness in all4 limbs, brisk reflexes in arms, absent in legsCombination of UMN and LMNClinical case 123, female presents to her GP with a 2 week history of bilateral leg weakness having started with pins and needles and numbness in her hands and feet. She has had a few days of urinary incontinence which has resolved. 2 years ago she had an episode of blurred vision and pain in the right eye which lasted a month and fully resolvedDiagnosis – MSVisual – optic neuritis, diplopia, nystagmus, internuclear opthalmoplegia, dysarthria, dysphagia, weakness, muscle spasms, ataxia, pain, paraesthesis, fatigue, cognitive impairment, depression, unstable moodUhthoff’s phenomenum – the worsening of neurological symptoms after periods of exercise and increased body heatLhermittes sign – an electrical sensation that spreads from the back into the limbs on neck flexion and or extensionBowel problems – incontinence, diarrhoea, constipationUrinary – incontinence, frequency, urinary retentionPlaques of demyelination within the CNS caused by an inflammatory process. Different areas of the CNS are involved over timeLP – cell count, protein, glucose and oligoclonal bands. WCC less than 50/mm3MRIVisual evoked potentions – show delayed conduction between the retina and the occipital cortexThere is no curative treatmentMultidisciplinary teamSymptomatic – spasticity, pain, fatigue, depression, continenceSteroids, beta interferon, glatiramer, natalizumabClinical case 261 femaleBecoming increasingly weak on her right side over a one week period. She is unable to walk and has slurred speech and right side of her face is droopingPast history of breast cancero/e – right facial weakness, grade 4/5 weakness of the right arm and leg, right homonymous hemianopia and some difficulty naming objects and reflexes are brisk on the right side and her right plantar response is upgoingdiagnosis = Cerebral maetastases from carcinoma of the breastCT head shows extensive oedema surrounding the subtle impression of a ring enhanced lesion in the left frontal lobe, extending into the left parietal lobe. There is associated mass effect displacing the lateral ventricleFeatures of raised intracranial pressure it is likely the oedema around the tumour has increased or bleedin has occurred within the tumourFeatures of raised ICP – visual loss, seizures and focal neurological deficit such as third and 6th cranial nerve palsiesMultidisciplary team, neurosurgery, corticosteroids, radiotherapy, chemotherapyCase 376 maleBackground of AF (on warfarin) has 2 hour history of severe global right sided weakness. He is eye-opening to painful stimuli and is moving his left side spontaneously. When questioned he seems confused12/15 E2, V4, M6Left hemisphere primary intracerebral haemorrhage causing right sided hemiparesisBloods tests, CXR, head CThead CT should have been performed within 24 hours or immediately in patients presenting with acute stroke if any of the following apply to them. – on anticoagulation treatment, known bleeding tendancy, decreased consciousness, papliodemea, neckstiffness or fever, severe headache with sudden onset, Ultrasound doppler, cerebral angiography, echocardiographyRisk factors – hypertension, smoking, DM, FH, increasing age, previous strokes, vascular disease, hyperlipidaemia, hypercoagulable state, alcohol abuse, malignancyIn ishcamic stroke – thrombolysis three hours from obsets are elegibleAspirin, lipid lowering drugs, anticoagulation if patient has AF or other source of embolusHaemorrhaging stroke – supprotive care. neurosurgeryCase 456 male6 month history of progressive weakness of his right hand. Also had problems with swallowing and has choked whilst eating on several occasionso/e he has wasting of his upper and lower limbs and some fasciculation's were noted his right plantar was up going and his reflexes were generally briskMotor neurone diseaseMRI – to exclude local brainstem pathologyEMG – acute denervation of the lower motor neuronesCases were the diagnosis isn’t clear – LP to exclude MS, muscle biopsy to exclude muscle disease. Blood tests for other conditions ................
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