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Phase 2
Kaveesha RajapaksaRyad Chebbout
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Pathology, Aetiology, Clinical Symptoms and Signs, Investigations and Management of:•Epilepsy•Multiple Sclerosis•Guillain-Barre Syndrome•Motor Neuron Disease•Parkinson's Disease•Dementia
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Aims
DefinitionRecurrent tendency to have spontaneous, intermittent and abnormal electrical activity in a part of the brain or generalised across the brain. Leading to seizures.
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Epilepsy
Aetiology1.Idopathic (2/3rds)2.Structural (Trauma, SOL, Developmental, Stroke)3.Metabolic (hypoglycaemia, hypocalcemia, hyponatraemia)
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Epilepsy
Partial = focal onset (localising features!)Generalised = no localising features!
Simple = awareComplex = impaired awareness
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Epilepsy
Partial SeizuresCommonly caused by structural pathology.
Simple Partial (Jacksonian March)Complex Partial = classically temporal lobe!Partial + Secondary Generalisation
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Epilepsy
Generalised SeizuresCommonly idiopathic.
Absence = </ 10sec, childhoodTonic-Clonic = complex, stiff->jerk, post-ictal confusion + drowsinessMyoclonic = sudden limb/face/trunk jerkAtonic = loss of tone->fall, no LOC
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Epilepsy
Prodrome – Aura – Ictal – Post-Ictal
ProdromeMood/Behaviour Change
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Epilepsy
AuraStrange Smell, Flashing Lights, Déjà vu/Jamais vu
Post-IctalHeadache, Confusion, Myalgia, Sore Tongue, Todds Palsy (hemiplegia), Dysphasia
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Epilepsy
Ictal – Localising FeaturesTemporal Lobe: Automatisms (lip smacking/fiddling), Visceral Aura (abdominal rising sensation), Dysphasia, Déjà vu/Jamais Vu, HallucinationsFrontal Lobe: Jacksonian March (tingling/muscle contractions from fingers to ipsilateral face), Todds Palsy
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Epilepsy
Parietal Lobe: Tingling Numbness
Occipital: Visual Phenomena (spots/lines/flashes)
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Epilepsy
InvestigationsEEG (classification)MRI (structural lesions)MEG/PET/SPECT ictal (localise epileptogenic focus for surgery)
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Epilepsy
Management
Partial = Carbamazepine
Generalised = Sodium Valproate OR Lamotrigine
Neurosurgical Resection
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Epilepsy
ManagementCounselling – employment, insurance, driving (1yr seizure free)
Contraception and pregnancy
Epilepsy Nurse Specialist
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Epilepsy
ComplicationsSudden Unexpected Death in Epilepsy (SUDEP)
Status Epilepticus
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Epilepsy
Discrete Plaques of Demyelination in Central Nervous System
T-cell Mediated
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Multiple Sclerosis
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Multiple SclerosisRisk Factors = Women, Temperate Areas
~30yrs
Demyelination Plaque (commonly periventricular, cervical spine, brain stem)Heals IncompletelyProlonged DemyelinationAxonal LossClinically Progressive Symptoms
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Multiple Sclerosis
Clinical Courses•Benign•Relapsing Remitting•Secondary Progressive•Primary Progressive
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Multiple Sclerosis
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Multiple SclerosisSymptoms
Monosymptomatic!
Disseminated in Time and Space
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Multiple SclerosisOptic Neuritis: Decreased Visual Acuity, Pain on Eye Movement, Dyschromatopsia
Sensory: Lhermittes Sign, Limb Numbness/Tingling
Motor: Transverse Myelitis, UMN Weakness, Uhthoff’s Phenomenon
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Multiple SclerosisOther: Ataxia, Erectile Dysfunction, Urinary retention
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Multiple SclerosisInvestigationDissemination in Time and Space!Clinically (attacks + clinical lesions, 2:2, 2:1, 1:1)+/- Aid of MRICSF (Oligoclonal Bands)Evoked Potentials
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Multiple SclerosisManagementAcute: Methylprednisolone IV
Chronic: Interferon/Glatiramer, Natalizumab
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Guillain-Barre SyndromeAcute AUI Inflammatory Demyelinating Polyneuropathy
Triggers: Campylobacter jejuni, CMV, Mycoplasma
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Guillain-Barre SyndromeSymptoms4 wk peak!
•Weakness – Leg, Trunk, Respiratory. Proximal, Distal. Symmetrical.•Back/Limb Pain•Autonomic Features: seating, tachycardia, arrhythmia’s.
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Guillain-Barre SyndromeSignsAreflexia!
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Guillain-Barre SyndromeInvestigationsNerve Conduction Studies – slow conductionRegular FVC
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Guillain-Barre SyndromeManagementIV Immunoglobin or Plasma Exchange
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Motor Neuron DiseaseSelective loss of motor neurons in: Motor Cortex (UMN), Cranial Nerve Nuclei (UMN/LMN) and Anterior Horn Cells (LMN).
>40yrs.
</10% Familial. ~20% SOD1 mutation.
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Motor Neuron DiseaseKey FeaturesUMN + LMN SignsNo Sensory Loss/Sphincter DisturbanceNo Eye Involvement
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Motor Neuron DiseaseClinical PatternsAmyotrophic Lateral SclerosisProgressive Bulbar Signs – CN IX-XII, bulbar/pseudobulbar palsyProgressive Muscular Atrophy – no UMN signsPrimary Lateral Sclerosis – mainly UMN
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Motor Neuron DiseaseAssociationsFronto-Temporal Dementia (10-35%)!
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Motor Neuron DiseaseSignsStumbling Spastic GaitFoot Drop +/- Proximal MyopathyWeak GripSpasticity/Hypereflexia/Upwards Plantars + Wasting/Fasciculations
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Motor Neuron DiseaseInvestigationsMRI/LP/Neurophysiology – exclude other causes
ManagementRiluzole – prolong life by ~ 3monthsSymptomatic + MDT (Ventilation, PEG)
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Parkinson's DiseaseDecreased Dopaminergic Neurons in Substantia Nigra (Pars Compacta)
Decreased Striatum Dopamine LevelsDecreased Basal Ganglia – Cortex CommunicationDecreased Movement
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Parkinson's Disease~65yrs. Associated with Lewy Bodies
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Parkinson's DiseaseClassic TriadTremor – resting, pill-rollingRigidity – increased tone, cogwheel rigidity, leadpipe rigidityBradykinesia – slowness of movement initiation-Expressionless Face, Monotonous Hypophonic Speech, Micrographia-Gait: Festinant, Reduced Arm Swing
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Parkinson's DiseaseOther SymptomsAnosmiaDepressionSleep disturbancesVisual Hallucinations (animals, children)Dementia (late stage)
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Parkinson's DiseaseManagementL-Dopa + Dopa-Decarboxylase Inhibitor (e.g. Madopar)-Efficacy reduces with time = Increased Dose-Dyskinesia’s, Off Freezing, End-of-Dose Reduced Relapse
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Parkinson's DiseaseManagementDopamine Agonist – Ropinirole/PramipexoleApomorphine – potent DA agonist, acuteAnticholinergics – tremor
Deep brain stimulation
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DementiaSyndrome of progressive deficits in 2 or more higher cognitive domains. (Memory, language, apraxia, agnosia, visuospatial function, personality)Interferes with social functioning.Occurs in clear consciousness. >80yrs=20%, >100yrs=70%
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DementiaTypesAlzheimer's DiseaseVascular DementiaLewry Body DementiaFronto-Temperal Dementia
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Alzheimer's DementiaIncreased Beta-Amyloid Peptide = Progressive Neuronal Damage (hippocampus, amygdala, temporal neocortex)-Neurofibillary Tangles-Amyloid Plaques-Decreased Ach
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Alzheimer's DementiaRisk FactorsFamily History, Downs Syndrome, Homzygosity for ApoE e4 Allele, DM/HTN/AF
Protective FactorsSmoking, Oestrogen
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Alzheimer's DementiaSymptomsProgressive Global Cognitive ImpairmentAphasiaAnosognosia (lack of insight)IrritabilityMood Disturbance – Depression, EuphoriaBehavioural Change – Wandering, Aggression
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Alzheimer's DementiaInvestigationsMMSE or Addenbrooks Cognitive ExamCT – temporal/parietal atrophy, ventricular enlargementMRI – hippocampus/amygdala/medial temporal lobe grey matter atrophyCSF – phosphorylated tau protein
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Alzheimer's DementiaManagementAcetylcholinesterase Inhibitors (Donepezil, Rivastigmine, Galantamine) – help lay down new memories
Memantine (Antiglutamatergic)
BP Control
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Vascular DementiaCumulative effect of many small strokes.
Vascular RF’s – Stroke Hx, HTN
Sudden Onset + Stepwise Deterioration -Emotional/Personality Changes-Cognitive Defecits-Depression/Labile Mood
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Lewy Body DementiaFluctuating Cognitive ImpairmentVisual Hallucinations (animals/children) +/- ParkinsonismRepeated Falls/Syncope
CT/MRI – relative sparing of medial temporal lobeHistology – Lewy Bodies in Brainstem/Neocortex
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Fronto-Temporal DementiaFrontal + Temporal Atrophy. AD Histology. Early, 45-65yrs
Behavioural/Personality ChangeDisinhibitionChange in Diet (sweets, overeating)Emotional BluntingPick bodies on histology
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DementiaManagementCare CoordinatorCapacityDevelop Routines, Plan AheadChallenging Behaviour – Lorazepam, Risperidone (not Lewy Body!)Depression - Citalopram
A 65 year old man with walking difficulties presented to his general practitioner. He complained of worsening tremor in the right arm with stiffness, which he said on occasion spread to his right leg. He said that the tremor was much worse when he was stressed, or in public. Examination revealed a man with a resting tremor, marked cogwheeling rigidity of the right side and an inability to perform repetitive tasks with the right arm. His gait was not normal and he had a reduced arm swing on the right.
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