Seizure for Medical Finals (based on Newcastle university learning outcomes)

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  • 8/14/2019 Seizure for Medical Finals (based on Newcastle university learning outcomes)

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    Hospital Based Practice Seizure.

    Abnormal movements. Movement disorders are typically heterogenous both clinically and pathologically. Characterized by impairment of movement.

    Planning Control Execution

    Examples of movement disorders include. Ataxia Dystonia Gait disorders Chorea Myoclonus Parkinsonism Spasticity

    Tardive dyskinesia Tics Tremor

    Tremor Note.

    Frequency Amplitude Exacerbating factors.

    StressFatigue

    Rest tremor. Abolished by voluntary movement. Seen in Parkinsonism

    Intention tremor. Irregular Large amplitude Worst at the end of purposeful acts. Suggests cerebellar disease.

    MSStroke

    Postural tremor. Absent at rest Present on maintained posture

    Arms stretch out in front of patient. May persist, but isnt exaggerated by, movment. Causes.

    Benign essential tremor. Autosomal dominant Reduced by alcohol

    ThyrotoxicosisAnxiety agonists.

    Re emergent tremor. Postural tremor that develops after a delay of about 10 seconds.

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    Seen in Parkinsonism. Asterixis.

    Coarse, non rhythmic hand flap. Worsened by extending arms and cocking back wrists Causes.

    Liver failureRenal failureCarbon dioxide narcosis.

    Management.SurgeryDeep brain stimulation.

    Chorea Non rhythmic, jerky and purposeless Flit from one place to another.

    Facial grimacing

    Raising shoulders Flexing and extending fingers

    Causes. Huntingdons Sydenhams Strep infection

    Rare complication.

    Hemiballismus. Large amplitude Flinging Hemichorea

    Affects proximal muscles. Contralateral to vascular lesion of subthalamic nucleus. Often occurs in elderly diabetics. Recovers spontaneously over months.

    Athetosis Slow Sinuous Purposeless

    Especially. Digits Hands Face Tongue

    Often difficult to distinguish from chorea. Commonest cause is cerebral palsy.

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    Tics Brief Repeated

    Stereotyped. Able to be suppressed for a while. Common in children.

    Usually resolve. Tourettes syndrome.

    Motor tics Vocal tics Management.

    Psychological supportIf tics are severe.

    Clonazepam Clondine Haloperidol.

    Risk of tardive dyskinesia.

    Myoclonus. Sudden Involuntary Jerky Generalised or focal Seen in.

    Metabolic problems.Eg. Renal failure

    Neurodegenerative disease.Eg. Lysosomal storage enzyme defects.

    CJD Myoclonic epilepsy. Benign essential myoclonus.

    General myoclonusBegins in childhoodAutosomal dominant inheritance.

    No other consequences.

    Myoclonus may respond to. Valproate Clonazepam Piracetam.

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    Tardive dyskinesia Occur after chronic exposure to dopamine receptor blockers.

    Antiemetics Antipsychotics.

    Can be permanent, even when causative drug is stopped. Can cause significant distress and disability. Classification.

    Tardive dyskinesia.OrobuccolingualTruncalChoreiform

    Eg. Chewing and grimacing movmements. Tardive dystonia.

    Sustained stereotyped muscle spasms.Twisting or turning character.Eg. Retrocollis & back arching.

    Tardive akathisiaUnpleasant inner sense of restlessness or unease.May also be repetitive, purposeless movementsEg. Stereotypes, pacing.

    Tardive myoclonus. Tardive Tourettism

    Tardive tremor.May respond to donepezil.

    Treatment Gradually withdraw neuroleptics. Wait 3 6 months before recommencing. Consider tetrabenazine 12.5 50 mg TDS PO Change antipsychotics to atypical that are less likely to cause tardive symptoms.

    QuetiapineOlanzapine.

    Dystonia Prolonged muscle spasm. Causes abnormal posture or repetitive movements. For example, writers cramp., inability to move hand to mouth. Can be classified by.

    Age of onset.Childhood is < 12 yearsAdolescence is 13 20 yearsAdulthood is > 20 years.

    Part of the body affected. Cause.

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    Childhood onset suggests idiopathic generalized dystonia. Often starts in one leg. Spreads to cover that side of the body over next 5 10 years. Often autosomal dominant condition.

    Often deletion in DTY1. Treatment is challenging.

    Exclude Wilsons diseaseExclude dopa responding dystonia

    Management.High dose trihexyphenidyl.

    Eg. benzhexol

    Anti cholinergic.Deep brain stimulation

    Dystonia may be confined to one part of the body, ie. A focal dystonia. Eg. Spasmodic torticollis (head pulled to one side). Blepharospasm. Writers cramp

    Focal dystonias in adults tend to be idiopathic. Rarely generalize Worsened by stress May develop geste antagonistique.

    To try and resist dystonic posturing.Eg. Touching finger to jaw in spasmodic torticollis.

    Effective control of focal dystonia is usually achievable with botox injections into thedysfunctioning muscle.

    May be side effects.

    Acute dystonia. May occur in young men who are starting neuroleptics. Clinical picture.

    Head pulled back Eyes drawn upwardsTrismus

    Management.Anti cholinergics.Eg. Benzotropine 1 2 mg IV.

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    Writers cramp. Look for.

    Hand and forearm spasm.Dystonic arm postureFocal tremor/ myoclonusDominant hand muscle hypertrophy

    Associated with OCD. EMG may show.

    Reduced reciprocal inhibition of wrist flexorsIncreased co contraction of antagonist forearm muscles during voluntarymovement.

    EEG may show abnormal motor command.Sensorimotor region region.

    Management.Simple measures often fail.

    blockers Valproate.

    Things that often work include. Arm cooling Breath holding Botox

    EMG biofeedback.

    Epilepsy. Recurrent tendency to spontaneous, intermittent, abnormal brain activity. Manifests as seizures. May take many forms.

    Tend to be stereotype for specific patient. Convulsions.

    Motor signs of electrical activity. Most normal patients would have convulsions under certain metabolic circumstances.

    Hyponatraemia

    Hypoxia Incontinence and myoclonic jerks are not particularly associated with epilepsy. Tongue biting and prolonged post ictal phase are very suggestative. Prevalence of active epilepsy is about 1%

    Clinical picture Prodrome lasting hours days.

    Rare.Change in mood or behaviour.

    Aura.Part of seizure.Strange feeling in abdomenSensation of dj vu.

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    Strange smellsFlashing lightsImplies partial seizure.

    Often Temporal lobe

    Partial motor seizures.Aka Jacksonian seizures.Temporary weakness of affected limb.

    Todds palsy. Post ictal period.

    MalaiseHeadacheMyalgiaConfusionSore tongue.

    Differential diagnosis of collapse. Stokes Adams attacks. Hypoglycaemia Orthostatic hypotension Drop attacks Anxiety Facticious blackouts Choking.

    Diagnosis Detailed description of the fit from a witness is vital.

    Be very cautious of diagnosing epilepsy in error.Major problem due to.

    Toxic drug side effects Stigmatising illness Employment problems. Expensive insurance Driving bans.

    Decide what type of fit it is. Main concern is with the onset of the attack. If the seizure starts with focal symptoms, it is partial.

    However fast it generalizes. Precipitants.

    Drugs TV

    Almost always generalizedRarely require drugs.

    Partial seizures. Features refer to a part of one hemisphere. Suggests structural disease. Elementary symptoms.

    Consciousness unimpaired.Eg. Focal motor seizure.

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    Complex symptoms.Consciousness impaired.Eg. Olfactory aura presceding autosomatism.Usually temporal lobe.

    Partial seizures with secondary generalisation.

    Electrical disturbances starting focally.Progresses to generalized seizure.

    Primary generalised seizures. No features referable to one hemisphere. Absences (petit mal).

    Brief (< 10 seconds) pausesEg. Suddenly stops talking in mid flow, then restarts where they left off.Presents in childhood.

    Tonic clonic.Classical grand mal seizure.Sudden onsetLoss of consciousnessLimbs stiffen (tonic) then jerk (clonic)May have tonic or clonic on their own.Drowsiness afterwards

    Myoclonic jerk.Eg. Thrown suddenly to the ground.Eg. Violently disobedient limb.

    Atonic/ akinetic.Becomes flaccid.

    Causes. Often none found. Structural.

    Trauma Space occupying lesion Stoke Tuberouls sclerosis SLE PAN Sarcoid Vascular malformations.

    Metabolic. Alcohol withdrawl. Benzodiaepine withdrawl Hyper or hypoglycaemia Hypoxia Uraemia Hypernatraemia Hypocalcaemia Liver disease.

    Drugs. Phenothiazides

    Tricyclics Cocaine

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    Infection. Encephalitis SYphiolis Cysticercosis HIV.

    Evaluation of a first seizure in adulthood. If in status epilepticus, manage as outlined later. Is it really the first fit?.

    Ask about previous.Funny turnsOdd behaviour Deja vu

    Odd episodic feelings of fear Is it really a seizure.?

    Convulsive syncopy is a common differential. Get a good, reliable history from a witness and the patient Beware unreliable witnesses reporting what they think you want to hear.

    Was the seizure provoked? Eg. Following

    Head injuryStrokeHyperglycaemiaAlcohol

    Drugs. Clozapine Tramadol Theophylline Baclofen

    Severe pyrexiaU&E dysfunction

    Provoked first seizures (symptomatic seizures)recur at a rate of 3 10%Unless due to underlying condition that cant be correct.edEg. Infarct, glioma

    Unprovoked seizures recur at rate of 30 50% Was there a trigger?

    Triggers are different to provocations.Strobe lightingTV

    Most people would have seizures if exposed to sufficient provocation, but would have no problem with triggers.

    Triggered attacks are diagnostic of epilepsy and tend to recur.

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    Investigations. Bloods.

    FBCU&ELFTsGlucoseCalcium

    PhosphateClottingAlcoholToxinsMedication levels

    Urine.Toxins

    Lumbar puncture.If CT rules out raised ICP.

    Imaging.CT

    If CTI normal, do MRI Allows detection of small cortical structural problems.

    Tumours Vascular malformations Cavernomas

    Dont image if it is likely that diagnosis is simple syncopy.EEG.

    Cant rule epilepsy in or out by itself. Helps classification and prognosis in first unprovoked seizure. Unequivocal epileptiform activity on EEG helps assess risk of

    recurrence. Only do emergency EEG if problem is non convulsive status

    epilepticus.

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    Management. Admit for 24 hours.

    Allows investigations.Allows monitoring of suspected pseudoseizure.

    Get prompt neurological help.Assist with diagnosis.Give individual concelling over employment, driving and dangers.

    Advise to stop driving and to contact the DVLA.Document your discussion.

    Consider treatment.If likely to recur.

    Unprovoked Structural lesion Status epilepticus Epileptiform EEG Post ictal Todds paresis.

    Partial seizure.

    Carbamazepine Lamotrogine Gabapentin Topiramate

    Generalized seizure. Valproate Lamotrigine Topiramate.

    Involve patients in all decisions.Compliance depends on communication and doctor patient relationship.Many patients will have issues with.

    Not wanting to stop driving Not being able to operate machinery Drug side effects Fear of sudden death.

    GPs tend to have about 50 epileptics on their books, so have more time tocounsel and support patients than neurologists, who have about 1500.

    Therapy. Normally start therapy after 2 or more fits.Discuss with pateient over risks of uncontrolled epilepsy against risks of drugs.Use monotherapy under control of one doctor.Slowly titrate up dose over 2 3 months until

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    Symptoms relieved Toxic effects are too severe. Maximum dose reached.

    Beware drug interactions.Match antiepileptic to character of seizure.

    Try all appropriate drugs singly at top dose before trying dual therapy.When changing drugs.

    Start new drug at minimum dose Slowly wean off old drug over 6 or so weeks. Remove old drug faster if toxicity was a problem

    Generalized. Try valproate as first line.

    Monitor LFTs & INR during first 6 months. Most hepatic failure occurs in patients < 3 years on

    polytherapy. Toxic effects.

    SedationTremor Weight gainHair thinningAnkel swellingHyperammonaemia

    EncephalopathyLiver failure.

    Drug levels arent helpful. If valproate not effective/ tolerated, try lamotrigine.

    May be more effective and better tolerated.Absence seizures.

    Valproate. Ethozuximide.

    Partial seizures generalization. Carbamazepine.

    Slow release form useful if side effects occur at peaks. Toxic effects include.

    Rash NauseaDiplopiaDizzinessFluid retentionHyponatraemiaBlood dyscrasias.

    2nd line. Valproate Levetiracetam Topiramate.

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    Phenytoin. Effective and well established. Not 1 st line due to toxicity.

    Nystagmus Diplopia Tremor Dysarthria Ataxia Decreased intellect Depression Poor drive Polyneuropathy Acne Coarse facial features Gum hypertrophy Blood dyscrasias

    Dosage is difficult & needs blood level monitoring.

    Lamotrigine. Useful monotherapy for primary generalized seizures.. Also used as add on in secondary generalized seizures. Halve monotherapy dose when combined with valproate. Double monotherapy dose when combined with carbamazipine or

    phenytoin. Side effects.

    Rash.May be serious

    Normally occurs within 8 weeks of starting therapy.Especially when co therapy with valproate.See doctor immediately if rash or flu symptomsassociated with hypersensitivity develops.Check.

    FBC U&E LFTs INR

    Fever Malaise Flu symptoms

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    Drowsiness Raised LFTs Photosensitivity Diplopia Reduced vision

    Vomiting Aggression Tremor Agitation Drug interactions

    Other anticonvulsantsAntimalarialsAntidepressants.

    Levetiracetam & Topiramate. New anti epileptics. Used for secondary generalized seizures.

    Side effects. Diarrhoea Vomiting Dyspepsia Depression Drowsiness Diplopia Neutropaenia.

    Zonisamide. Partial seizures Secondary generalized seizures.

    Weaning off of anti epileptics. Discuss pros and cons with patients. Most patients are seizure free within a few years of therapy. 50% remain seizure free if drugs are withdrawn. Trial off anti epileptics may be tried if patient has.

    Normal neurology Normal IQ Normal EEGSeizure free for 2 years

    No juvenile myoclonic epilepsy Some drug doses can be reduced by 10% every 2 4 weeks.

    CarbemazipineLamotriginePhenytoinValproateVigabatrin

    Others can be reduced by 10% every 4 8 weeks.PhenobarbitoneBenzodiazepinesEthosuximide

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    Enzyme inducers and contraception. Non enzyme inducers have no effect on the Pill.

    ValproateGabapentin

    LamotrigineLevetiracetam

    Other drugs require daily oestrogen (50 g OD), reduce pill free days from 7 to 4 and usecondoms.

    CarbamazepinePhenytoinPhenobarbitalPrimidone.

    An alternative is converting to Depo Provera.Enzyme inducers have no effect.

    Emergency contraception can be achieved with.

    CoilLevonorgestrel. Pre conception councelling and anti epileptics.

    Councelling is vital due to teratogenicity. Give high dose folic acid (5mg OD) from pre conception to delivery.

    Sudden unexpected death (SUDEP) Most common in uncontrolled epilepsy. May be related to seizure associated apnoea at night. Epilepsy patients have a death rate 3 times that of controls.

    About 700 epilepsy associated deaths occur in the UK every year.

    About 120 of these are SUDEP. There are support groups for those bereaved by epilepsy.

    Status Epilepticus. Seizure lasting > 30 minutes. Continuous seizures without regaining consciousness. Length of attack increases.

    Mortality Risk of permanent brain damage.

    Aim to terminate seizures as soon as possible.

    Status normally occurs in known epileptics. 50% have structural brain lesions if it is the first presentation.

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    Diagnosis of clonic status is normally quite easy. Diagnosis of status consisting of abscence or partial seizures can be difficult.

    Subtle eye movements Other signs of partial seizures.

    Investigations. EE|G can be very helpful. Check for pregnancy.

    If positive, then diagnosis is likely o be eclampsia.Check urine and BPCall senior obstetrician.Immediate delivery may be required.

    Telemetry Bloods.

    GlucoseBlood GasesU&ECalciumFBCAnticonvulsant levelsToxicology screenBlood cultures

    Management. Basic Life Support. Get IV access. Lorazepam.

    Beware respiratory arrest during end of infusion with all benzodiazepines.Alternative is diazepam.

    Less long lasting. Can also be given rectally.

    Buccal midazolam can also be given. Phenytoin.

    If fits continue lorazepamBeware hypotensionContraindicated if

    Bradycardia Heart block

    Monitor. BP ECG

    Diazepam.If fits continue after phenytoin

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    Requires close monitoring. Especially of respiratory function.

    Very rare for status not to respond once this stage of protocol is reached. If no response, consider pseudoseizure.

    Particularly if odd features such as.

    Pelvic thrustsResisting attempt to open lids.Resisting attempts to passive movementsFlailing arms and legs.

    Further management. Dexamethasone.

    If it is possible that seizures are due to. |Vasculitis Cerebral oedema Tumour.

    General anaesthesia.Requires admission to ITU.

    As soon as seizures are controlled.Start oral drugsDetermine the cause.

    Open and maintain airwayLay in recovery position

    Remove false teeth if poorly fitting

    Give 100% oxygen + suction as required.

    IV access and take bloods.

    FBC, U&E, LFTs, Glucose, Calcium, toxicology,anticonvulsant levels.

    Thiamine 250 mg IV over 10 minutes if alcoholism or malnourishment suspected.

    50 mL 50% dextrose unless glucose known to be normal

    Correct hypotension with fluids.

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    Guillain Barre syndrome. Incidence of 1 2/100.000/ year Causes

    Occurs a few weeks after infection or flu vaccineOften.

    Campylobacter jejuni CMV Mycoplasma Herpes Zoster HIV EBV

    No cause found in 40% Pathology causes antibody formation that attacks nerve cells.

    Clinical picture Develops over about 4 weeks.

    Gradually recovers. Muscle weakness that is

    AscendingSymmetricalTends to affect

    Proximal muscles. Trunk Respiratory muscles

    Respiratory failure is main danger. Cranial nerves

    Especially facial nerve Pain is common

    Eg.back or limb Sensory signs may be absent Autonomic dysfunction

    SweatingTachycardiaBlood pressure changesDysrhythmias

    Investigations.

    Nerve conduction studies.Slowed conduction

    Lorazepam slow IV bolus to stop seizures.

    IV infusion phase.Phenytoin 15 mg/kg at < 50 mg/minDiazepam 8 mg/hour in 5% dextrose.

    General anaesthesia phase.

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    Lumbar puncture.Protein often increased to > 5.5 g/L

    Normal CSF WCC

    Treatment. Respiratory involvement requires transfer to ITU.

    Ventilate sooner than later. FVC < 1.5 L PaO2 < 10 kPa PaCO 2 > 6 kPa

    Check FVC ever 4 hours IV immunoglobulins

    For 5 days. Plasma exchange Corticosteroids have no role.

    |Prognosis. Good

    85% make a complete recovery. 10% are unable to walk alone at 1 year Mortality of 10%

    Carpal tunnel syndrome. Commonest cause of hand pain at night. Due to compression of the median nerve as it passes under flexor retinaculum. Aggravated by.

    Pregnancy The Pill Myxoedmea Lunate fracture.

    Rare Rheumatoid arthritis Cardiac failure Premenstrual. Repetitive action Night time

    Clinical features. Median nerve distribution is affected.

    ThumbIndex finger

    Middle finger Tingling or pain

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    Flicking or shaking of the wrist brings relief. Pain can cause clumsiness Tinels test.

    Tapping over carpal tunnel produces parasthesia. Phalens test.

    Hyperflex wrist for 1 2 minutes.Positive test when hyperflexion reproduces the pain.More reliable than Tinels test.

    Later.Wasting of thenar eminenceDecreased sensation over lateral 3.5 fingers.

    Lateral palmar sensation is spared as palmar cutaneous nerve doesntrun through carpal tunnel.

    Tests.

    Nerve conduction studies not normally needed.May be negative anyway.

    Treatment. Carpal tunnel injections.

    Not certain if there is any benefit over placebo beyond 1 month. Wrist splints at night.

    May relieve nocturnal pain. Flexor retinaculum division.

    Decompresses carpal tunnel.Gives more permanent result.