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.
 Stress
 Fatigue
• Rest tremor.
○ Abolished by voluntary movement.
○ Seen in Parkinsonism
• Intention tremor.
○ Irregular
○ Large amplitude
○ Worst at the end of purposeful acts.
○ Suggests cerebellar disease.
 MS
 Stroke
• Postural tremor.
○ Absent at rest
○ Present on maintained posture
 Arms stretch out in front of patient.
○ May persist, but isn’t exaggerated by, movment.
○ Causes.
 Benign essential tremor.
• Autosomal dominant
• Reduced by alcohol
 Thyrotoxicosis
 Anxiety
 β – agonists.
• Re – emergent tremor.
○ Postural tremor that develops after a delay of about 10 seconds.
 ○ Seen in Parkinsonism.
• Asterixis.
○ Coarse, non – rhythmic hand flap.
○ Worsened by extending arms and cocking back wrists
○ Causes.
 Liver failure
 Renal failure
 Carbon dioxide narcosis.
○ Management.
 Surgery
 Deep brain stimulation.

Chorea
• Non – rhythmic, jerky and purposeless
• Flit from one place to another.
○ Facial grimacing
○ Raising shoulders
○ Flexing and extending fingers
• Causes.
○ Huntingdon’s
○ Sydenham’s
○ 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.
Tics
• Brief
• Repeated
• Stereotyped.
• Able to be suppressed for a while.
• Common in children.
○ Usually resolve.
• Tourette’s syndrome.
○ Motor tics
○ Vocal tics
○ Management.
 Psychological support
 If 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 myoclonus
 Begins in childhood
 Autosomal dominant inheritance.
 No other consequences.
• Myoclonus may respond to.
○ Valproate
○ Clonazepam
○ Piracetam.
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.
 Orobuccolingual
 Truncal
 Choreiform

 Eg. Chewing and grimacing movmements.

○ Tardive dystonia.
 Sustained stereotyped muscle spasms.
 Twisting or turning character.
 Eg. Retrocollis & back arching.
○ Tardive akathisia
 Unpleasant inner sense of restlessness or unease.
 May also be repetitive, purposeless movements
 Eg. 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.
 Quetiapine
 Olanzapine.

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 years
 Adolescence is 13 – 20 years
 Adulthood is > 20 years.
○ Part of the body affected.
○ Cause.
• 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 Wilson’s disease
 Exclude 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.
○ Writer’s 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 the
dysfunctioning muscle.
 May be side effects.

• Acute dystonia.
○ May occur in young men who are starting neuroleptics.
○ Clinical picture.
 Head pulled back
 Eyes drawn upwards
 Trismus
○ Management.
 Anti – cholinergics.
 Eg. Benzotropine 1 – 2 mg IV.
 • Writer’s cramp.
○ Look for.
 Hand and forearm spasm.
 Dystonic arm posture
 Focal tremor/ myoclonus
 Dominant hand muscle hypertrophy
○ Associated with OCD.
○ EMG may show.
 Reduced reciprocal inhibition of wrist flexors
 Increased co – contraction of antagonist forearm muscles during voluntary
movement.
○ EEG may show abnormal motor command.
 Sensorimotor region β region.
○ Management.
 Simple measures often fail.
• β – 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 abdomen
 Sensation of déjà vu.
  Strange smells
 Flashing lights
 Implies partial seizure.
• Often Temporal lobe

○ Partial motor seizures.

 Aka Jacksonian seizures.
 Temporary weakness of affected limb.
• Todd’s palsy.
○ Post – ictal period.
 Malaise
 Headache
 Myalgia
 Confusion
 Sore 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 generalized
 Rarely require drugs.
• Partial seizures.
○ Features refer to a part of one hemisphere.
○ Suggests structural disease.
○ Elementary symptoms.
 Consciousness unimpaired.
 Eg. Focal motor seizure.
 ○ 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) pauses
 Eg. Suddenly stops talking in mid – flow, then restarts where they left off.
 Presents in childhood.
○ Tonic – clonic.
 Classical grand mal seizure.
 Sudden onset
 Loss of consciousness
 Limbs 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
 • 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 turns
 Odd 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 injury
 Stroke
 Hyperglycaemia
 Alcohol
 Drugs.
• Clozapine
• Tramadol
• Theophylline
• Baclofen
 Severe pyrexia
 U&E dysfunction
○ Provoked first seizures (symptomatic seizures)recur at a rate of 3 – 10%
 Unless due to underlying condition that can’t be correct.ed
 Eg. Infarct, glioma
○ Unprovoked seizures recur at rate of 30 – 50%
• Was there a trigger?
○ Triggers are different to provocations.
 Strobe lighting
 TV
○ 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.
• Investigations.
○ Bloods.
 FBC
 U&E
 LFTs
 Glucose
 Calcium
 Phosphate
 Clotting
 Alcohol
 Toxins
 Medication 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
• Don’t image if it is likely that diagnosis is simple syncopy.
 EEG.
• Can’t 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.
• 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 Todd’s 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 to
counsel 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
 • 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.
 Sedation
 Tremor
 Weight gain
 Hair thinning
 Ankel swelling
 Hyperammonaemia
• Encephalopathy
 Liver failure.
○ Drug levels aren’t 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
 Nausea
 Diplopia
 Dizziness
 Fluid retention
 Hyponatraemia
 Blood dyscrasias.
• 2nd line.
○ Valproate
○ Levetiracetam
○ Topiramate.
 Phenytoin.
• Effective and well established.
• Not 1st 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 – symptoms
associated with hypersensitivity develops.
 Check.
• FBC
• U&E
• LFTs
• INR
○ Fever
○ Malaise
○ ‘Flu symptoms
 ○ Drowsiness
○ Raised LFTs
○ Photosensitivity
○ Diplopia
○ Reduced vision
○ Vomiting
○ Aggression
○ Tremor
○ Agitation
○ Drug interactions
 Other anticonvulsants
 Antimalarials
 Antidepressants.
 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 EEG
 Seizure – free for 2 years
 No juvenile myoclonic epilepsy
○ Some drug doses can be reduced by 10% every 2 – 4 weeks.
 Carbemazipine
 Lamotrigine
 Phenytoin
 Valproate
 Vigabatrin
○ Others can be reduced by 10% every 4 – 8 weeks.
 Phenobarbitone
 Benzodiazepines
 Ethosuximide
 • Enzyme inducers and contraception.
○ Non – enzyme inducers have no effect on the Pill.
 Valproate
 Gabapentin
 Lamotrigine
 Levetiracetam
○ Other drugs require daily oestrogen (50 µg OD), reduce pill free days from 7 to 4 and use
condoms.
 Carbamazepine
 Phenytoin
 Phenobarbital
 Primidone.
○ An alternative is converting to Depo Provera.
 Enzyme inducers have no effect.
○ Emergency contraception can be achieved with.
 Coil
 Levonorgestrel.
• 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.
• 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 BP
 Call senior obstetrician.
 Immediate delivery may be required.
○ Telemetry
○ Bloods.
 Glucose
 Blood Gases
 U&E
 Calcium
 FBC
 Anticonvulsant levels
 Toxicology screen
 Blood 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 lorazepam
 Beware hypotension
 Contraindicated if
• Bradycardia
• Heart block
 Monitor.
• BP
• ECG
○ Diazepam.
 If fits continue after phenytoin
  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 thrusts
 Resisting attempt to open lids.
 Resisting attempts to passive movements
 Flailing 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 drugs
 Determine the cause.

Open and maintain airway

Lay 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.

 Lorazepam slow IV bolus to stop seizures.

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

General anaesthesia phase.

Guillain – Barre syndrome.
• Incidence of 1 – 2/100.000/ year
• Causes
○ Occurs a few weeks after infection or ‘flu vaccine
 Often.
• 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
 Ascending
 Symmetrical
 Tends 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
 Sweating
 Tachycardia
 Blood pressure changes
 Dysrhythmias

• Investigations.
○ Nerve conduction studies.
 Slowed conduction
 ○ 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
• PaCO2 > 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.
 Thumb
 Index finger
 Middle finger
○ Tingling or pain
 ○ Flicking or shaking of the wrist brings relief.
○ Pain can cause clumsiness
○ Tinel’s test.
 Tapping over carpal tunnel produces parasthesia.
○ Phalen’s test.
 Hyperflex wrist for 1 – 2 minutes.
 Positive test when hyperflexion reproduces the pain.
 More reliable than Tinel’s test.
○ Later.
 Wasting of thenar eminence
 Decreased sensation over lateral 3.5 fingers.
• Lateral palmar sensation is spared as palmar cutaneous nerve doesn’t
run 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.