Neuro CBLS Flashcards
A 29-year-old woman is brought to A and E by her husband.
She has been convulsing on and off for ~ 45 minutes with partial recovery between episodes.
Her epilepsy, which started four years ago, has never been controlled with medication and this is her third such presentation to A and E in the last six months despite her being on high doses of two anti-epileptic drugs - carbamazepine and levetiracetam.
2 diagnostic possibilities
-
Non-Epileptic status
- change in mental status or behaviour from baseline, associated with continuous seizure activity on EEG
-
Convulsive Status Epilepticus
- seizure > 5mins
- no recovery in between seizures
How might you distinguish GCSE and NES
Generalised convulsive status epilepticus with non-epileptic status
- Movement
- Cardiorespiratory status
- Conscious level
GCSE
- rhythmic clonic jerking
- cyanosis
- deeply unconscious
NES
- arrhythmic flailing, stop start
- pink
- resistance to eye opening
- gaze aversion
- responsiveness during stop phases
- emotional post ictal phase
Who gets PNEAD and why?
PNEAD = psychologically derived non-epileptic attack disorders
- majority are young women wo have experienced abuse in childhood
- trauma conditions the brain to dissociate and this manifests by somatic symptoms
PNEAD management and role of neurologist
- Explain to patient symptoms are real but are not due to structural disease in the brain
- attacks occurring at a sub conscious level
- over stress may trigger
- PNEAD is treatable
a. neuropsychologist : to identify whether she can connect remote trauma to her current symptomsb. psychiatrist : recommend drug treatment for mood disturbance or anxiety or both
56 M , BIBA, AED
pc: convulsion, fluttering sensation in chest before losing consciousness.
witness: his wife says his puts his hand on his chest, his eyes flicker rapidly and he shakes uncontrollably “like a very bad tremor.”
breathing can be erratic but not cyanosed
hpc: 3rd episode in 1 month
pmh: pacemaker in situ since having an inferior MI nine months previously
likely diagnosis
Late onset psychogenic non-epileptic attacks
- may be triggered by life changing physical health problems
- patients often have insight into origin of the problem and are responsive to psychological interventions
What are refractory seizures:
- ongoing seizures despite two I.V treatments
- one of which is a benzodiazepine AND 2nd line treatment within 30 mins
- HDU / ITU input
STATUS EPILEPTICUS
What if the first dose of Lorazepam doesn’t stop the seizures:
Second can be given.
If seizures continue for 15 mins —> 2nd line treatment will be needed
PHENYTOIN (slow infusion with cardiac monitoring)
If seizures continue for 30 mins
- refractory status —> ITU
- anaesthesia and sedation
Typical presentation of GBS
- Symmetrical ascending weakness (feet moves up body)
- Reduced reflexes
- Peripheral loss of sensation or neuropathic pain
- May progress to cranial nerves and cause facial nerve weakness
Criteria for diagnosis of GBS
BRIGHTON CRITERIA
Investigations which may support diagnosis of GBS
-
Nerve conduction studies
- reduced signal through the nerves
- demyelination leading to acute inflammatory demyelinating poly radiculo neuropathy
-
Lumbar puncture for CSF
- raised protein?
- normal cell count and glucose?
- rule out infection
CYTOALBUMINIC DISSOCIATION
Management of GBS
- IV immunoglobulins
- Plasma exchange
- supportive care
- VTE prophylaxis (PE)
- Intubation and Ventilation in respiratory failure
What would be the difference between a patient with classical locked in syndrome and a patient with severe GBS?
Locked in syndrome
-
pontine infarction
- CN3,4 come out of midbrain so vertical movements of eyes preserved
- pontine controls horizontal eye movements (abducens, CN 6)
Patient would be able to undertake vertical eye movement and eyelid opening (cn3,4)
Who is involved in the neurorehabilitation unit:
- Occupational therapists
- upper limb posture, movement, dexterity - Physio
- supporting weak joint
- strengthening resp muscles - SALT
- optimise speech and swallowing - NURSES AND HCA
- therapy sessions - Psychologist
- emotional support - Dieticians
- dietary needs, route of feeding - Rehab doctors
- oversee the rehab team
- manage symptoms and medication
Cotton wool spots in eye indicate
lack of blood flow to small retinal blood vessels
Key features of Temporal lobe seizures
- with or without impairment of consiousness
- aura!
- 1 min (lip, smacking, grabbing, plucking)
Key features of frontal lobe seizures
Head / leg movements
Posturing
Post ictal weakness
JACKSONIAN MARCH: patient does not lose awareness
Key feature of seizure in parietal lobe
Sensory, paraesthesia
Key features of seizure in occipital lobe
- floaters / flashes
Area of brain which involves comprehension
WERNICKES AREA
Management for high blood pressure
LABETALOL
- beta blocker
- and acts on alpha adrenoreceptors reducing vascular resistance
Does upper motor neuron lesion have forehead sparing or not?
UPPER = forehead sparing
Type of brain aneurysm commonly caused by chronic hypertension
Charcot-Bouchard aneurysm
56 Male, HTN, T2DM suddenly declines with severe headache, nausea and intermittent vomiting
key investigations
CT brain without 12 hours
- need to exclude SAH
Thunderclap headache and no blood on CT scan would indicate need for Lumbar puncture after 12 hours:
- allow haemoglobin ring to metabolised to the yellow coloured bilirubin (xanthochromia)
- needs to be transported in a light protected container because bilirubin is broken down by UV light
What are the principles of management of a patient with confirmed spontaneous subarachnoid haemorrhage?
Identify presence of aneurysm with CT Brain
- endovascular coil embolization
- clipping
What are complications of subarachnoid haemorrhage and how might these be managed?
Manage complications:
1. SAH —> sympathetic storm —> excess catecholamines being released —> HTN, t.cardias, GI ischaemia (peptic ulcers and bowel infarction)
- NOTE ABOUT HTN: normal autoregulation of cerebrals can be lost hence HTN may be tolerated by clinicians. Hypotension could lead to profound ischaemia and stroke.
- MAP targets in first week of SAH = 80-90mmHg
- Hydrocephalus (tx w/ lumbar drain or repetitive LPs)
- Hyponatraemia
- due to SAIDH? - delayed cerebral ischaemia (DCI)
- VASOPASM
- blood products —> release of inflammatory cytokines
- inflammatory response facilitates blood vessel spasm —> spasm reduces further blood loss. However the spasm reduces delivery of blood to the rest of the healthy brain
- CEREBRAL ISCHAEMIA
What is given to prevent vasospasm in brain?
calcium channel blocker (nimodipine)
Treatment of subdural haematoma
In the acute setting
- acute A-E assessment
- anti-epileptics (1 week after presentation of SHD)
- Trauma craniotomy
- large opening in the skull to create evacuate the haematoma and relieve the associated mass effect
- Decompressive craniotomy
- bone flap may be left out at surgery.
Management of chronic SDH
Burr Hole craniotomy with irrigation or twist drill craniotomy with drain placement
Differential diagnoses for decline in conscious level
AEIOU TIPS
A-alcohol
E-epilepsy
I-insulin
O-overdose
U- uraemia (renal failure)
T- trauma
I - infection (sepsis)
P - psychiatric condition
S - stroke / shock
What does the brain require to maintain consciousness?
- Reticular activating system
- Brainstem
- Cerebral cortex
Brain requires glucose and oxygenated blood at perfusion pressure of 50-60mmHg
Formula for cerebral perfusion pressure:
CPP = Mean arterial pressure - Intracranial pressure
GCS
Motor Response
6 = obeys commands
5 = localises to pain
4 = withdraws from pain
3 = abnormal flexion to pain (decorticate)
2 = extending to pain
1 = none
Verbal response
5 = orientated
4 = confused
3 = words
2 = sounds
1 = none
Eye opening
4 = spontaneous
3 = to speech
2 = to pain
1 = none
Uncal herniation management
1. URGENT INTUBATION FOR AIRWAY protection
—-> ANAESTHESIA
a) reduces depolarisation of neurons so reduces the energy demand in a situation where oxygen limited.
b) reduces blood supply, reduces intracranial blood volume —> lowers ICP
2. OSMOTHERAPY
—–> Mannitol or hypertonic saline
a) reduce ICP
b) may stimulate v. constriction –> reducing ICP
3. CT scan
Commonest cause of extradural haematoma
middle meningeal artery
Treatment for tonic or atonic seizures
M - SODIUM VALPROATE
F - lamotrigine
Generalised tonic clonic treatment
M = sodium valproate
F = lamotrigine / Leve
Focal seizures treatment
1st line = Lamotrigine / Leve
2nd line = carbamazepine, oxcarbazepine, zonisamide
What AED may exacerbate absent seizures
carbamazepine
Treatment for absent seizures
1st line = ethosuximide
2nd line =
MALE - sodium valproate
FEMALE - lamotrigine
Treatment for myoclonic seizures
Males - sodium valproate
Females - leve
Mnemonic for potentially life threatening headaches
SNOOP
S- systemic signs and disorder
N-neurologic symptoms
O- onset new or changed and patient > 50
O- onset in thunderclap presentation
P- papilloedema, pulsatile tinnitus, positional provocation, precipitated by exercise
Migraine acute treatment
Acute treatment:
Simple analgesia
- Aspirin 900 mg or
- Ibuprofen 400mg or
- Paracetamol 1000 mg
+/- Triptan (Oral sumatriptan first choice)
+/- antiemetic (metoclopramide 10 mg or prochlorperazine 10 mg)
Migraine prophylaxis treatment
- PROPRANOLOL
- TOPIRAMATE (teratogenic)
- Acupuncture (10 sessions over 5 weeks)
Not in guidelines
Candesartan
Monoclonal antibodies against CGRP
Cluster headache management
Acute
100% oxygen
Subcutaneous triptan
Prophylaxis
VERAPAMIL
Tension type headache treatment
Acute treatment: aspirin, paracetamol or NSAID first line
Prophylaxis
- up to 10 sessions of acupuncture over 58 weeks
- low dose amitriptyline
Temporal arteritis investigations
- raised inflammatory markers ESR > 50
- temporal artery biopsy
Treatment of temporal arteritis
Treatment : ASAP don’t wait for biopsy
If no vision loss → HIGH DOSE PRED
Vision loss→ IV METHYL PRED
URGENT OPTHAL REVIEW
Management for trigeminal neuralgia
- Carbamazepine is 1st line
- Failure to respond to treatment or atypical features should prompt referral to neurology
Key features of subdural haematoma
Key features
- Age
- Trauma
- Fluctuating confusion
- Decreased consciousness
- Anticoag use
- Alcohol use
acute subdural haematoma treatment
- trauma craniotomy flap to evacuate haematoma
larger acute subdural haematoma w/ mass effect
- decompressive craniotomy
chronic subdural haematoma treatment
burr hole craniotomy
key investigations for subarachnoid haemorrhage
non-contrast CT head 1st line
LP if CT normal after 12 hours
Management of subarachnoid haemorrhage
MX
NEUROSURGERY URGENT REFERRAL
Supportive: rest, analgesia, VTE prophylaxis
NIMODIPINE - stop vasospasm
Surgery - Coil or clipping !
Extradural haemorrhage management
MX
URGENT NEUROSURGERY REFERRAL
Conservative (<30cm3, minimal midline shift, GCS > 8 w/o focal neurological deficits)
SURGICAL
—> Craniotomy , Burr Holes
—> Ligate / cauterise bleeding source
LUCID INTERVAL
