SDH, EDH and epilepsy Flashcards Preview

Neurology > SDH, EDH and epilepsy > Flashcards

Flashcards in SDH, EDH and epilepsy Deck (28):

SDH - definition

This is a treatable condition that should be considered in a patient with a fluctuating conscious level or in those having an ‘evolving stroke’ – especially those on anticoagulants.


SDH - bleeding and risk factors

Bleeding – bridging veins between the cortex and venous sinuses are vulnerable to de-acceleration resulting in an accumulating haematoma between the dura and the arachnoid mater. This gradually increases ICP, pushing the midline structures away and leading to tentorial herniation and coning.

Risk factors – the elderly are more susceptible due to brain atrophy making bridging veins vulnerable. Other risk factors include history of falls (e.g. in epileptics or alcoholics) and anticoagulation.    


SDH - symptoms and signs

Symptoms – can emerge up to 9 months after an event – fluctuating level of consciousness, insidious physical or intellectual slowing, unsteadiness, sleepiness, headache or personality changes.

Signs – raised intracranial pressure (headache, drowsiness, vomiting, pupil changes or papilloedema), seizures or localising neurological symptoms e.g. hemiparesis (occurring mean 63 days after injury).


SDH - differential diagnosis

Stroke, dementia or CNS masses – tumours or cerebral abscess.


SDH - investigations

CT or MRI shows the clot and midline shift – look for crescent shaped collection of blood over 1 hemisphere – the sickle shape differentiates subdural from extradural haemorrhage.


SDH - management

Evacuation1st line is burr twist drill or hole craniostomy and 2nd line is craniotomy.


EDH - definition and bleeding

When blood accumulates between the dura mater and the bony skull. Suspect an EDH after a head injury if conscious level falls or is slow to improve or if there is a lucid interval.

Bleeding – usually due to a fractured temporal or parietal bone causing laceration of the middle meningeal artery and vein. This typically occurs after trauma to a temple just lateral to the eye.


EDH - symptoms

The lucid interval may last a few hours to a few days before the patients GCS begins to fall caused by raised ICP – severe headache, vomiting, confusion and seizures typically follow with or without focal neurological signs – hemiparesis with brisk reflexes and an up-going plantar. If bleeding continues – ipsilateral pupil dilation, coma, bilateral limb weakness and deep and irregular breathing.


EDH - differential diagnosis

Epilepsy, carotid dissection (spontaneous or traumatic) or CO poisoning.


EDH - investigations

CT shows a lens shaped haematoma (more rounded shape than SDH) and skull x-ray may show evidence of fracture lines crossing the course of the middle meningeal vessels.


EDH - management

Stabilise and transfer urgently to a neurosurgical unit for clot evacuation ± ligation of the bleeding vessel. Starting an IVI of mannitol (osmotic agent) can help reduce the raised ICP.


Epilepsy - definition

A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain which manifests as seizures. Convulsions are the motor signs of electrical discharge.


Elements of a seizure

  • Prodrome – a change in mood or behaviour that can occur in hours to days before the seizure. 
  • Aura – part of the seizure of which the patient is aware – could be strange feeling in stomach, déjà vu (sense of familiarity), strange smells or flashing lights – implies a partial seizure. 
  • Post-ictally – headache, confusion, myalgia, a sore tongue, temporary weakness following a focal motor cortex seizure or temporary dysphasia following a focal temporal seizure.


Partial seizures

Focal onset with features referable to a part of one hemisphere:

  • Simple partial – awareness is unimpaired with focal motor, sensory (e.g. olfactory or visual), autonomic or psychic symptoms. There are no post-ictal symptoms. 
  • Complex partial – awareness is impaired and seizures most commonly arise in the temporal lobe and cause post-ictal confusion. Frontal seizures have a rapid recovery. 
  • Partial with secondary generalisation – in 2 thirds of patients with partial seizures the electrical disturbance spreads causing a 2° generalised seizure – usually convulsive.


Generalised seizures

Simultaneous onset of electrical discharge throughout the cortex.

  • Absence – brief (<10 secs) pauses e.g. stop in mid-sentence – presents in childhood.
  • Tonic clonic – loss of consciousness when limbs stiffen (tonic) and then jerk (clonic). 
  • Myoclonic – a sudden jerk of the limb, face or trunk – patient may fall to the ground. 
  • Atonic – a sudden loss of muscle tone causing a fall with no loss of consciousness.


Localising features of a partial seizure

  • Temporal lobe – complex motor phenomena (e.g. lip smacking, chewing, fumbling, singing or violence), rising abdominal sensation or pain, dysphasia, memory phenomena (e.g. déjà vu or jamais vu), emotional involvement (e.g. terror, anger or elation) or delusional behaviour. 
  • Frontal lobe – motor features e.g. posturing or peddling movements of the leg, Jacksonian march – spreading focal motor seizure starting in the face or thumb, subtle behavioural disturbances, dysphasia or speech arrest or post-ictal Todd’s palsy (persistant weakness). 
  • Parietal lobe – mainly a sensory disturbance e.g. tingling, numbness or pain. 
  • Occipital lobe – visual phenomena such as spots, lines and flashes of light.


Causes of seizures

  • Structural – cortical scarring (e.g. head injury years before onset), developmental (e.g. cortical dysgenesis), space occupying lesion, stroke, hippocampal sclerosis or vascular malformation. 
  • Non-epileptic causes of seizure – trauma, stroke, haemorrhage, raised ICP, alcohol or benzo withdrawal, metabolic disturbance, liver disease, infection or drugs (e.g. tricyclics or cocaine).


Diagnosis of epilepsy

  • Are these really seizures? – a detailed description from a witness is vital and wonder whether they are reliable or not? Tongue biting and a slow recovery are very suggestive features. 
  • What types of seizures are they? – partial or generalised – the onset of the attack is the key. 
  • What triggers them? –  such as alcohol or flickering lights of a TV (rarely require treatment).


Epilepsy - investigations

EEG alone cannot be used to exclude or confirm epilepsy but can help with the diagnosis and classification of a seizure. Other useful tests include MRI to look for structural lesions, serum drug levels to assess drug compliance and MEG or PET to help localise epileptogenic focus.


Epilepsy management - counselling

Advise against possible dangers e.g. swimming, driving or heights until a diagnosis is established. After diagnosis individualised counselling is needed re employment, insurance and conception. Patients should inform the DVLA and not drive until seizure free for >1 year.


Epilepsy management - AEDs

Most specialists would not recommend treatment after one fit unless risk of reoccurrence is high e.g. structural brain lesion, focal neurological deficit or unequivocal epileptiform EEG. Treatment should be started after the second seizure.  

  • Generalised tonic-clonic - 1st line is Sodium valproate amd 2nd line is Lamotrigine. 
  • Absence - 1st line is Sodium valproate and 2nd line is Lamotrigine. 
  • Tonic, atonic or myoclonic  - 1st line is Sodium valproate and 2nd line is Lamotrigine. 
  • Partial with 2° generalisation - 1st line is Carbamazepine and 2nd line is Sodium valproate.


Epilepsy management - valproate

Initially give 300mg BD and increase by 100mg BD every 3 days up to a maximum of 30mg/kg daily.

Side effects – ALPROATE - increased appetite, liver failure, pancreatitis, reversible hair loss (grows back curly), oedema, ataxia, teratogenicity, tremor, thrombocytopenia or encephalopathy (due to hyperammonaemia).


Epilepsy management - lamotrigine

As monotherapy initially give 25mg OD and increase by 50mg OD every 2 weeks up to a max of 500mg per day. Half monotherapy dose if on valproate and double if on carbamazepine or phenytoin.

Side effects – maculopapular rash in 10%, Stevens-Johnson syndrome in 1 in 1000, hypersensitivity, diplopia, tremor or vomiting.


Epilepsy management - carbamazepine

Initially give 100mg BD and increase by 100mg BD every 2 weeks up to a max of 1000mg BD.

Side effects – leucopenia, diplopia and impaired balance.


Epilepsy management - phenytoin

No longer first line due to toxicity – nystagmus, diplopia, tremor and side effects – decreased intellect, depression, coarse facies, acne or gum hypertrophy.


Epilepsy further management

  • Neurosurgical resection – can be used where a single epileptogenic focus can be identified – 70% chance of success but risk of causing future neurological deficits. 
  • Vagal nerve stimulation – can reduce seizure frequency and severity in 33% patients.


Women with epilepsy

  • Teratogenicity of AEDs – avoid sodium valproate (give lamotrigine) and take 5mg folic acid OD. 
  • Pre conception counselling – vital due to the 5% risk of fetal abnormalities. 
  • Breastfeeding – most are present in breast milk but lamotrigine is not thought to be harmful. 
  • Contraception – non-enzyme inducing AEDs have no effect on the pill – this includes sodium valproate and lamotrigine. With other AEDs >50μg of oestrogen may be required.


Stopping AEDs

Discuss risks and benefits with the patients – most patients are seizure free within a few years of starting and 50% remain so when drugs are withdrawn. 

Criteria for withdrawal – normal neuro examination and IQ, normal EEG, seizure free for >2 years and no juvenile myoclonic epilepsy.

One way to withdraw the AEDs is to decrease the dose by 10% every 2-4 weeks.