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(Cardiff University Clinical Neuroscience Society) 09..11.2O23 PT NEUROLOGY MADE EASY Christopher Watanabeharief, Kudakwashe Rusenza,Topics Topic 1: Stroke Topic 2: Demyelinating Disease Topic 3: Cranial Nerve PathologiesSTROKE Stroke by definition is a clinical syndrome consisting of rapidly developing clinical signs of focal and potentially global disturbances of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of a vascular origin. The cerebral function issues causing there to be parts of the brain that are starved of oxygen. Stroke is a general term and can present in 2 different ways: ischemic stroke and haemorrhagic strokeISCHEMIC STROKE ischemic stroke can be caused by several blood flow to the affected brain region leading to inadequate tissue perfusion. Examples of these mechanisms include: embolism thrombosis cerebral venous thrombosis HAEMORRHAGIC STROKE In terms of haemorrhagic stroke, there is only two main subtypes : subarachnoid haemorrhagee bleeding is due to a ruptured blood vessel, this Suoutside the brain tissue, between the pia matter and the can be with in the brain tissue or with in the arachnoid matter. ventricles CLASSIFICATION OF STROKE Tinitial symptoms using the Bamford classificationthe total anterior circulation stroke - all three must be system. present This system requires assessment of 3 main things: partial anterior circulation stroke - 2 out of the three Unilateral hemiparesis /hemi-sensory loss of the must be present Homonymous hemianopia Higher cognitive dysfunction – e.g., dysphagia or visuospatial disorder posterior circulation stroke- one of the following must be present : · Cranial nerve palsy and a contralateral motor/sensory deficit · Bilateral motor/sensory deficit · Conjugate eye movement disorder (e.g. horizontal gaze palsy) · Cerebellar dysfunction (e.g., vertigo, nystagmus, ataxia) · Isolated homonymous hemianopia LOCATING THE LESION anterior cerebral artery stroke Posterior cerebral artery stroke stroke in the branches of the posterior cerebral artery that supply the midbrain. Posterior inferior cerebellar artery stroke basilar artery strokeebral artery strokeACUTE STROKE INVESTIGATIONS AND MANAGEMENT SECONDARY STROKE MANAGMENT anti-platelet therapy: Lipid modification drug treatment: all patients should be placed on this Unless contraindicated, treatment with a high-intensity statin (such The standard treatment is as atorvastatin 20–80 mg daily) will be offered at diagnosis of clopidogrel 75 mg daily. ischaemic stroke or TIA by secondary care. Aspirin 75 mg daily with modified- retwice daily may be used if clopidogrel cannot be tolerated. Modified-release dipyridamole Antihypertensive drugs: 200 mg twice daily may be used if Treatment for hypertension following stroke or TIA should be both clopidogrel and aspirin are initiated by secondary care following diagnosis and may include a contraindicated or cannot be thiazide-like diuretic, long-acting calcium-channel blocker, tolerated. angiotensin-converting enzyme inhibitor, or angiotensin-II Aspirin 75 mg daily may be used if receptor blocker. both clopidogrel and modified-release Blood pressure targets for people with CVD are the same as for dipyridamole are contraindicated or people without CVD, except for people with severe bilateral cannot be tolerated carotid artery stenosis, for whom a systolic blood pressure target of 140–150 mmHg is appropriate.SBA 1 Question- Which of the following best describes the effect of an ischaemic stroke in the anterior, middle and posterior cerebral arteries? A. ACA: impaired judgment, upper limbs affected, paraesthesia MCA: hemiparesis of lower ipsilateral face, peripheral vision loss, PCA: dysphagia, ataxia, nystagmus B. ACA: contralateral lower limb weakness MCA: hemiparesis of lower contralateral face, speech impairment, contralateral weakness, PCA: acute vision loss, memory loss language dysfunction, PCA: Gait apraxia, bitemporal hemianopia, deafnessausea, D. ACA : contralateral upper limb weakness ,MCA: contralateral lower limb weakness ,PCA: bitemporal hemianopia E. ACA: hemiparesis of lower contralateral face, speech impairment, contralateral weakness, MCA: acute vision loss, confusion, memory loss, PCA: contralateral lower limb weakness, urinary incontinence SBA 1 EXPLANATIONS B the ACA supplies the medial portions of the frontal lobes and superior medial parietal lobes, which are involved in lower limb supply and - therefore occlusion to this artery will cause contralateral lower limb weakness. The MCA supplies areas of the frontal, temporal and parietal lobes including the areas responsible for facial, throat, and hand/arm innervation (both sensory and motor), hence occlusion causes speech impairment, contralateral weakness and hemiparesis of the lower contralateral face (this is forehead sparing supplies the occipital lobe which is involved in visual processing, hence PCA stroke can present with acutePCA vision loss. Memory impairment occurs due to hippocampal infarction (as the hippocampus is supplied by the PCA).SBA 2 Question.- A 56-year-old man presents to the emergency department with sudden medical history of a transient ischaemic attack 6 months ago and type 2 diabetes mellitus. On examination, there is ptosis of the left eyelid and the left eye is shifted downward and laterally. There is reduced power and sensation in the upper and lower right limbs. A cerebellar examination is unremarkable however the patient reports feeling nauseated during past-pointing assessment due to his double vision. A. lateral medullary syndrome B.lateral pontine syndrome C. locked in syndrome D. Horner’s syndrome E. Weber’s syndromeSBA 2 EXPLANATIONS Answer explanations. This patient has presented with cranial nerve III palsy and right-sided hemiparesis. This is consistent with the midbrain stroke termed 'Weber's syndrome’. Horner’s does not cause weakness, although it will cause the ptosis. lateral medullary would cause - ipsilateral facial loss of temperature and pain sensation, contralateral limb loss of temperature and pain sensation and weakness, ataxia and nystagmus. ipsilateral facial weakness, loss of temperature and pain sensation, contralateral limb weakness and loss of temperature and pain sensation. This would also have deafness in the patient . And finally, we can exclude locked in syndrome as this would cause complete paralysis below the eyes but this patient is able to move despite being weak. ByKudaRusenza NeuromuscularDisordersDefinition: “Widerangeofdiseasesaffectingthe PNS,whichconsistsofallmotorand sensorynervesthatconnectthebrain andspinalcordtotherestofthebody. Progressivemuscleweaknessisthe predominantconditioninthese disorders.”MotorNeuronDisease(MND) Diseaseofthemotor neurons ->onlymotor neuronsaffectedinHx Unknowncause Variouspatternsofdisease: Amyotrophic Lateral Sclerosis (ALS) Progressivemuscularatrophy BulbarPalsyMND–KeyFeatures Asymmetriclimbweakness(ALS) UMN+LMN Fasciculations Nosensorysigns Rarely<40yo RarelyFHxofMNDorclosely relatedconditione.g. frontotemporaldementiaMND-Symptoms Weaknessinankleorleg Slurredspeech Weakgrip Musclecrampsortwitches Weightloss Difficultystoppingyourselflaughingin inappropriatesituations Suddenuncontrollablecrying Uncontrollableexcessiveyawningsometimes evenwhennottired DifficultybreathingMND-Diagnosis Clinical->testsdonetoexcludeothercauses Nerveconductionstudies->Normal Electromyogram(EMG)->reducedno.of AP+increasedamplitude MRI->excludedifferentials LP Bloodtests MuscleBiopsy(rare) Genetest(sometimesforcause) No cure MND-Treatment Conservative Medical SurgicalConservative MDT Doctor Specialistnurse Physiotherapist(PT) OccupationalHealth(OT) SpeechandLanguageTherapy (SALT) Dietician Emotionalsupport(you+carer)Medical Diseaseprogression Riluzole Musclecramps Quinine Musclestiffness Baclofen Drooling Alternativeoptionsdeskinpatch Communicationdifficulty Communicationaids Swallowingdifficulty CarbocisteineoracetylcysteineforthicksecretionsSurgical SwaGastrotomytubelty Difficultybreathing Non-invasiveventilation(NIV)MS Chroniccell-mediatedautoimmune disorder Inflammatorycellsattackcellsofthe whitematterofCNS Lesionsonwhitematter Resultsinscarringhencenamemultiple sclerosis Causes: Unknown Virale.g.EBVMS-Symptoms Visual Uhthoff’sphenomenon Sensory Pinsandneedles TrigeminalNeuralgia Motorhermitte’ssign PredominantlyUMN(canalsobeLMN) Cerebellar Ataxia+tremor Other Sexualdysfunctionce IntellectualdeteriorationPatternsofprogressionMS-Investigation CNExam Fundoscopy ECG Bloods BM* B12/folate* Syphilis* Vasculitis NMO Imaging->MRIbrainandspine(+/- gadolinium) Dorsan’sfingersplaques Juxtacorticalhypertintensity Tonometry->IOP MS-Specialtests LP Oligoclonalbands eyes Glucose Protein WCC VisualEvokedPotentialsMS–Diagnosis McDonald'scriteria Disseminationintimeand spaceMS– Management Conservative Medical SurgicalConservative MDT Physician PT OT SALT Nurses Supportgroups VTEprophylaxis VitD Medical Acute Long-term 1stline->MethylprednisoloneoralorIV Oralbetter–moreconvenient+cheaper immunosuppressantreatments(DMTs)– PPIcoveriforal Alemtuzumab Ocrelizumab Bloodborneviralscreenbeforestarting MonitorIgGlevelsandWCC Surgical DeepBrainStimulation–tremorsand stiffness Rhizotomy–Trigeminalneuralgia Baclofenpump–spasticity HematopoieticStemcelltransplant–very rare Resetimmunesystemtostopit attackingyourCNS NIV–breathingdifficulties Gastrotomy–dysphagiaMyastheniaGravis(MG) Autoimmune–AcetylCholineReceptors AsThymomas-15% Autoimmunedisorder:perniciousanaemia,thyroid,rheumatoid,SLE Thymichyperplasia50-60% MorecommoninwomenMG-KeyFeatures Extraocularmuscles:Diplopia Proximalmuscleweakness Face Neck Limbgirdle Ptosis Dysphagia Weakness worse on increased movement and relieved by restMG-Investigations Bloods Anti-acetylcholineantibodies-85-90%patients Anti-muscle-specifictyrosinekinaseantibodies CK–normal SinglefibreEMG(sensitivity92-100%) CTthorax Notcommon->Tensilontest IVedrophoniumtemporarilyreducesweaknessMG–Management Long-termacetylcholinesterase inhibitors 1ˢᵗline->Pyridostigmine Immunosuppressants Prednisolone Alternatives:Azathioprine, cyclosporine,mycophenolate mofetil SurgThymectomy Myastheniccrisis Treatment: Complication of MG -> worsening muscle weakness, resulting in respiratory failure Plasmapheresis that requires intubation and mechanical IVIG ventilationLambertEaton Myasthenic Syndrome(LES) Paraneoplastic->Small Cell Lung Cancer Mayalsooccur independentlyas autoimmunedisorder Autoimmuneattackofpre- synapticvoltage-gated Ca²⁺channelsinPNSLES-KeyFeatures Limbgirdleweakness(lowerlimbfirst) Hyporeflexia Autonomicsymptoms: Drymouth Impotence Difficultyurinating Ophthalmoplegia* Ptosis* Increased strength with repeated muscle contractions –50%pts *Not common RuleoutMG EMG LES– Investigations Incrementalresponsetorepetitiveelectrical stimulation Lookforcancer Bloods ChestXRandCT Pleuralaspirate+/-sputumsample(ifpossible) Biopsy(ifindicated) BronchoscopyLES–Management Treatmentofunderlyingcancer Immunosuppressants Prednisolone Azathioprine Trialeddrug->3,4-Diaminopyridine IVIG+plasmapheresismaybebeneficialGuillainBarreSyndrome (GBS) Triggeredbyinfection:nationofPNS Campylobacter jejuni Mycoplasmapneumoniae CMV EBV Zikavirus Cross-reactionofantibodieswith gangliosidesinthePNSGBS–KeyFeatures Back/legpaininitially–65%pts PrClassicallyascendingi.e.legsfirstfalllimbs Reduced/absentreflexes(LMN) Veryfewmildsensorysignse.g.distalparaesthesiaGBS–Otherfeatures Hxofgastroenteritis Respiratorymuscleweakness Cranialnerveinvolvement Bilateralfacialnervepalsy Oropharyngealweaknessiscommon Autonomic Urinaryretention Diarrhoea Papilloedema–reducedCSFresorptionMiller-Fisher Syndrome Associatedwith: Ophthalmoplegia Areflexia Ataxia Eyemusclestypicallyaffectedfirst Descendingparalysisratherthan ascendingGBS– Investigations Bloods GM1in25%pts)sideantibody(e.g.anti- Anti-GQ1bforMiller-Fishervariant– 90%pts LP Raisedprotein NormalWCC Nerveconductionstudies Decreaseinmotornerveconduction Prolongeddistalmotorlatency IncreasedFwavefrequencyGBS–Management Conservative Supportivecare Medical 1ˢᵗline->IVIG Alternative:Plasmapheresis Nosurgical Immunoglobulinreducesseveritynot lengMostrecoverin6-12months VariesinsomepatientsSBA1 A30-year-oldfemalecameintotheemergency departmentpresentingwithnewonsetdoublevision, fatigueandarmweakness.Shenoticedherweakness getsworseparticularlytowardstheendofthedayand thatshe’sbeenfeelingmoreshortofbreathafter minimalexerciserecently.Onexamination,younoticed shehaddiplopia.Whatisthemostsensitivetestforthe singlemostlikelydiagnosisinthispatient? a.MRIbrainandspine b.Anti-acetylcholineantibody c.Single-fibreelectromyogram d.Lumbarpuncture e.TensilontestSBA1 A30-year-oldfemalecameintotheemergency departmentpresentingwithnewonsetdoublevision, fatigueandarmweakness.Shenoticedherweakness getsworseparticularlytowardstheendofthedayand thatshe’sbeenfeelingmoreshortofbreathafter minimalexerciserecently.Onexamination,younoticed shehaddiplopia.Whatisthemostsensitivetestforthe singlemostlikelydiagnosisinthispatient? a.MRIbrainandspine b.Anti-acetylcholineantibody c.Single-fibreelectromyogram d.Lumbarpuncture e.TensilontestSBA1Explanation ThispatientislikelytohaveMyasthenia Gravis.Shepresentswithprogressivemuscle weaknessworseattheendofthedayafter repetitiveuse.Thisisalsoaffecting respiratorymuscleasshegetsmorefatigued withlessexercise.Shealsohasdiplopiaand andptosiswhicharecharacteristicsigns. ThesinglemostsensitivetestforMGisa single-fibreEMGwithasensitivityof92- 100%andanormaltesteffectivelyrulesout MG.SBA2 A39-year-oldfemalewasadmittedtotheneurologyward followinganepisodeofsevereeyepainandneurological deficit.Shedescribesapreviousepisode6monthsearlier whichwasslightlysimilarbutlesssevere.Afterseveraltest wereperformed,adiagnosisofMultipleSclerosiswas confirmed.Thepatientwasconcernedaboutwhatthiswill meanforherfutureandhowthiswillprogress.Whatisthe bestdescriptionforthemostcommontypeofprogression seeninMS? a.Unpredictableattackswhichultimatelyleaveno permanentdamage. b.Unpredictableattackswhichmayormaynotleave permanentdamage. c.Steadyandcontinuousdeteriorationoffunctionwith superimposedattacks. d.Steadyandcontinuousdeteriorationoffunction. e.Steadyandcontinuousdeteriorationoffunction followingunpredictableattackswhichmayormaynot leavepermanentdamage. SBA2 A39-year-oldfemalewasadmittedtotheneurology wardfollowinganepisodeofsevereeyepainand neurologicaldeficit.Shedescribesapreviousepisode 6monthsearlierwhichwasslightlysimilarbutless severe.Afterseveraltestwereperformed,a diagnosisofMultipleSclerosiswasconfirmed.The patientwasconcernedaboutwhatthiswillmeanfor herfutureandhowthiswillprogress.Whatisthe bestdescriptionforthemostcommontypeof progressionseeninMS? a.permanentdamage.ackswhichultimatelyleaveno b.Unpredictableattackswhichmayormaynotleave permanentdamage. c.Steadyandcontinuousdeteriorationoffunction withsuperimposedattacks. d.Steadyandcontinuousdeteriorationoffunction. e.Steadyandcontinuousdeteriorationoffunction followingunpredictableattackswhichmayormay notleavepermanentdamage.SBA2ExplanationSBA3 A42-year-oldmalecameintotheneurologyoutpatient departmentpresentingwithfrequentfalls,inabilityto swallowproperlyforthelast3daysanddoublevisionwith blurring.Patienthadnoticedthefallspriortohisvisual symptoms,hehadbilateralptosis,abnormallateralgazein botheyesandweakhandgrip.Onaskinghimtowalkina straightline,hefailedtodoso.Onfurtherexamination,you couldelicitnoreflexesandfound somedistallimb paraesthesia.Hehadnopastmedicalhistoryotherthana recentepisodeofgastroenteritiswhichresolvedin3days twoweeksprior.Giventhefindings,whatisthesinglemost likelydiagnosis? a.MultipleSclerosis b.MotorNeuroneDisease c.GuillainBarreSyndrome d.Parkinson’sDisease e.MillerFisherSyndromeSBA3 A42-year-oldmalecameintotheneurologyoutpatient departmentpresentingwithfrequentfalls,inabilityto swallowproperlyforthelast3daysanddoublevisionwith blurring.Patienthadnoticedthefallspriortohisvisual symptoms,hehadbilateralptosis,abnormallateralgazein botheyesandweakhandgrip.Onaskinghimtowalkina straightline,hefailedtodoso.Onfurtherexamination,you couldelicitnoreflexesandfound somedistallimb paraesthesia.Hehadnopastmedicalhistoryotherthana recentepisodeofgastroenteritiswhichresolvedin3days twoweeksprior.Giventhefindings,whatisthesinglemost likelydiagnosis? a.MultipleSclerosis b.MotorNeuroneDisease c.GuillainBarreSyndrome d.Parkinson’sDisease e.MillerFisherSyndromeSBA3Explanation Thispatientpresentswithneurological symptomsfollowinganepisodeof gastroenteritiswhichishighlysuggestiveof GuillainBarreSyndrome.Thispatientalso presentedwithabnormallateralgazeinboth eyes,noreflexesanddifficultywalking consistentwiththeclassictriadofavariantof GBS-Miller-FisherSyndrome (ophthalmoplegia,areflexia,ataxia).OtherNMDisorders Peripheralneuropathies Musculardystrophy MyopathyMarieTooth Dermatomyositis Polymyositis SubacuteDegenerationoftheSpinalCord Syringomyelia SpinalMuscularAtrophyCRANIAL NERVE REVISION 1 CN I - smell sensation CN II - vision pupil constriction (pupillary sphincter muscle), eyelid opening (levator palpebrae), accommodation (ciliary muscle) CN IV - eye movement (SO - depression) somatosensation of the anterior 2/3rd of theion, tongue, dampening of loud noise (tensor tympani) CN VI - eye movement (LR - abduction)CRANIAL NERVE REVISION 2 CN VII - muscle of facial expression, eye closing (orbicularis oculi), dampening of loud noise (stapedius), taste sensation from anterior 2/3rd tongue (chorda tympani), lacrimation, salivation (submandibular & sublingual) CN VIII - hearing, balance CN IX - taste sensation from posterior 1/3rd tongue, swallowing, salivation (parotid gland), elevating pharynx & larynx, monitoring of carotid body & sinus CN X - taste sensation from supraglottic region, soft palate elevation, midline uvula, talking, cough reflex, monitoring of aortic arch CN XI - head-turning, shoulder shrugging CN XII - tongue movementCN III, IV, VI PALSY GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) CN III palsy caused by posterior communicating artery aneurysm, cavernous sinus problem (infection, tumour infiltration, thrombosis) CN IV & VI palsy caused by diabetes mellitus or ocular trauma PRESENTING COMPLAINT CN III palsy - eye looks “down and out”, double vision, ptosis, proptosis, fixed dilated pupil CN IV palsy - eye looks “up and out”, double vision worse in vertical plane, may tilt their head upward to compensate CN VI palsy - eyes looks inward, double vision worse in horizontal planeINTERNUCLEAR OPHTHALMOPLEGIA (INO) GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) Caused by lesion in the median longitudinal fasciculus (MLF) responsible for control of horizontal gaze Lesion. is caused by MS or cerebrovascular accidents PRESENTING COMPLAINT Impaired adduction during horizontal gaze Retains ability to converge to nearby targetsINTERNUCLEAR OPHTHALMOPLEGIA (INO) INVESTIGATIONS Neuroimaging in this case MRI to identify brainstem lesion CSF & LP if MS is suspected MANAGEMENT Depends on the cause identifiedSBA 1 An 80-year-old male patient presents to the emergency department with a 1 hour history of sudden onset of double vision after he hit himself hard against a lampost. On physical examination, he reports that the double vision is worse when looking down and gets better when tilting his head to the left side and there is a bruise around his eye. Which of the following is the most accurate clinical diagnosis? A. Right 4th nerve palsy B. Left 4th nerve palsy C. Cavernous sinus thromboembolism D. Compression of cavernous sinus secondary to pituitary adenoma E. Multiple SclerosisSBA 1 EXPLANATIONS C & D would present with symptoms such as headache, photophobia, diplopia and would have CN III palsy presentation E would present with painful eye Hitting the eye means ocular trauma is likely and CN IV nerve palsy would be more consistent. On physical exam, looking to the left helps reduce diplopia so the lesion is more likely on the right side. So the answer is ASBA 2 A 42-year-old female with a background of multiple sclerosis attends the neurology clinic for a follow-up. unable to adduct her left eye and nystagmus is noted in the right eye on abduction.atient is Which option best describes this abnormality? A. Lesion in left frontal eye field B. Lesion in right paramedian pontine reticular formation C. Right internuclear opthalmoplegia D. Left internuclear opthalmoplegia E. Left CN VI nerve palsySBA 2 EXPLANATIONS A would present with patient’s both eyes looking towards the left side B would present with patient’s both eyes looking away from the right side C would present with inability to adduct the right eye and nystagmus on the left eye D would present with inability to adduct the left eye and nystagmus on the right eye, which fits the description and so is correct E would present with left eye looking inwardsTRIGEMINAL NEURALGIA GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) Chronic pain condition This is seen more in women over the age 50 The cause can be primary (idiopathic), secondary (malignancy, AVM, MS, sarcoidosis, Lyme disease) PRESENTING COMPLAINT Unilateral facial pain described as “shooting” or “stabbing” Triggered by light touch, eating, wind blowing on face etcTRIGEMINAL NEURALGIA INVESTIGATIONS Usually a clinical diagnosis But neuroimaging can be used to exclude secondary cause MANAGEMENT Medical : 1st line: carbamezapine, 2nd/3rd line: phenytoin, lamotrigine Surgical: microvascular decompression (relocate the blood vessel in contact with CN V), alcohol injection (damage the CN V), removal of tumours/AVM etc RARE NEURALGIA Glossopharyngeal neuralgia - pain in tongue, ear, throat Occipital neuralgia - pain in back of the head or neckFACIAL NERVE PALSY GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) Dysfunction of CN VII It can be unilateral (or sometimes bilateral) The cause can be CNS involvement (lesion in motor cortex or area connecting motor cortex & CN VII nuclei), acoustic neuroma, trauma, systemic infection or inflammation (Lyme’s disease or sarcoidosis), Ramsay Hunt Syndrome, mononeuritis multiplex PRESENTING COMPLAINT Unilateral or sometimes bilateral Altered sense of taste facial weakness or paralysis Decreased salivation and lacrimation Difficulty closing the eye Loss of nasolabial fold HyperacusisBELL’S PALSY GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) Caused is unknown But viral infection particularly HSV-1 reactivation has been implicated PRESENTING COMPLAINT Acute & Unilateral Affecting forehead Not affecting muscles of mastication & extraocular muscles Mild to moderate post-auricular otalgia Other symptoms are same as CN VII palsyFACIAL NERVE PALSY INVESTIGATIONS Clinical examination Imaging like CT & MRI to rule out structural lesion Serology MANAGEMENT Antiviral agent for Ramsay Hunt syndrome Antibiotics for Lyme disease Surgical intervention for acoustic neuroma & trauma Rehabilitation to restore facial muscle function Corticosteroid (PO 50 mg Prednisolone OD for 10 days) ± Aciclovir for Bell’s PalsyISCHAEMIC STROKE AFFECTING CRANIAL NERVE BASILLAR ARTERY STROKE Ocular CN Nuclei affected Loss of horizontal eye movements LATERAL PONTINE SYNDROME Paralysis of face, Altered taste sensation, Decreased salivation & lacrimation WALLENBERG’S SYNDROME (AKA LATERAL MEDULLARY SYNDROME) Nucleus Ambiguus (CN X, XI, XII) affected Dysphagia, Hoarseness of voice, Absent Gag reflex BULBAR PALSY PSEUDOBULBAR PALSY GENERAL FACTS (PATHOLOGY, EPIDEMIOLOGY) Lower motor neurone lesion Upper motor neurone lesion affecting cranial nerve nucleirve or cortex to cranial nerve nucleiom motor Caused by brainstem stroke Caused by bilateral internal capsule & tumours, degenerative stroke, degenerative (MND, progressive (ALS), autoimmune (GBS) supranuclear palsy), autoimmune (MS) Both affects CN IX, X, XII PRESENTING COMPLAINTSBA 1 A 71 year old man presents to his GP with ringing in his left ear. Upon asking he mentions that he has experienced similar episodes before and also had felt as though world is spinning around. On examination, he has a left-sided facial droop, impaired hearing on the left, and otoscopy reveals a vesicular rash in his auditory canal. What is the likely diagnosis? A. Bell’s palsy B. Drug induced ototoxicity C. Ménière's disease D. Vestibular schwannoma E. Ramsay Hunt syndromeSBA 1 EXPLANATIONS The patient presents tinnitus & vertigo And facial nerve palsy, herpetic rash, hearing loss on examination. A would cause facial nerve palsy but would not explain the other symptoms B would cause vertigo and hearing loss but would not cause facial nerve palsy C would cause tinnitus, hearing loss, vertigo but would not cause facial nerve palsy D & E could cause almost all the symptoms, but only E could explain the rash in the auditory canal as this rash is caused by varicella zoster reactivation so E is correctSBA 2 dysphagia, difficulty speaking, and emotional lability. A few months ago she had a self- limiting episode of limb weakness and urinary incontinence. On physical examination there is slow speech, spastic tongue and a brisk jaw jerk reflex. Which of the following pathophysiological mechanisms best explains the underlying cause? A. Ischaemic stroke affecting bilateral internal capsule B. Antibodies against nicotinic ACh receptors C. Demyelination of the cortico-bulbar white matter tract D. Ischaemic stroke affecting MCA E. Ischaemic stroke affecting PICASBA 2 EXPLANATIONS The patient presents with dysphagia, difficulty speaking, emotional lability And spastic tongue and brisk jaw jerk reflex on examination. emotional labilityr limb paralysis and aphasia but doesn’t typically cause CN abnormality and E would cause Wallenberg syndrome which commonly present with Horner’s syndrome as well B would cause myasthenia gravis A & C would both cause pseudobulbar palsy. But A would be a more acute onset C would be relapsing & and remitting (as it is MS) like the patient described so C is correctFollow us on: Thank you for coming to Instagram our teaching session! Slides will be provided once you have completed the feedback form Facebook