1. Disorders affecting consciousness Flashcards
what are the two groups of disorders that affect consciousness
episodic loss (or alteration) of consciousness
persistent alteration of consciousness
give some examples of episodic loss/alteration of consciousness
seizure
syncope (vasovagal/cardiogenic)
non-epileptic attack (pseudoseizure, dissociative attack)
give some examples of causes of persistent alteration of consciousness
encephalopathy - “brain dysfunction”
encephalitis - “brain infection or inflammation”
raised ICP
what are the clinical features of a seizure
use: triggers preceding symptoms blanks fall ictus duration post-ictal
triggers - rare
preceding symptoms - sensoral, psychic, tomato-sensory, auras, motor
blanks - dissconection or abrupt loss
fall - fast, tonic
ictus - tonic clonic, tonic
duration - GTCS 30s-5m, Secondarily GTCS ~62s
post-ictal - confusion, somnolence, headache
what are the clinical features of syncope
use: triggers preceding symptoms blanks fall ictus duration post-ictal
triggers - frequent
preceding symptoms - N/V, visual blurring, epigastric pain, heat, headache, tinnitus
blanks - fading away
fall - slow, flacid
ictus - flaccid, tonic anoxic seizure
duration - ~15s (3-30s)
post-ictal - somnolence, headache
what are the clinical features of a non-epileptic attack
use: triggers preceding symptoms blanks fall ictus duration post-ictal
triggers - stressful situation (but may be none)
preceding symptoms - hyperventialtion, panic, none
blanks - variable
fall - variable
ictus - motionless, variable thrashing movements
duration - usually >5mins, often much longer
post-ictal - variable
what are the two groups of seizures
focal
primary generalised
what are the three types of focal seizures
simple partial - no loss of awareness
complex partial - loss of awareness
secondary generalised - focal that spread resulting in a tonic clonic seizure
what are the three types of primary generalised seizures
tonic-clonic
absences
myoclonic
what is the definition of epilepsy
more than one seizure
what is the lifetime prevalence of any seizure compared to % of people with epilepsy
lifetime prevalence of any seizure = 1-2%
epilepsy = 0.5-1%
what are risk factors for epilepsy
Family history
Focal brain damage / pathology
e.g. stroke, tumour, meningitis, trauma, learning difficulty
Toxins, drug withdrawal, infection, metabolic disturbance (e.g. hypoglycaemia)
Sleep derivation
All LOWER SEIZURE THRESHOLD
what is important to know when making a diagnosis of epilepsy
GOOD HISTORY
From patient and eye witness
- before the attack, prodrome, during the attack, after the attack
what investigations can be done for epilepsy
MRI (gold standard) CT EEG ECG routine bloods
what is the treatment for epilepsy
Treat risk factors if possible e.g. reduce / stop alcohol
Usually drug therapy if > 1 seizure
- 2/3rds with epilepsy respond well to treatment
- 1/3rd more difficult and resistant to treatment
what are some common drugs used in epilepsy
Sodium valproate (Epilim)**
Carbamazepine (Tegretol)
Lamotrigine
Phenytoin**
Leviteracetam **
Topiramate
Gabapentin / Pregabalin
Phenobarbitone
**available for IV use
what is the Glasgow coma scale
GCS used to assess consciousness in a patient
scored from 3-15 over 3 areas - eye opening, verbal response, motor response
what is the scoring for eye opening in the GCS
4 - spontaneous
3 - to speech
2 - to pain
1 - none
what is the scoring for verbal response in the GCS
5 - orientated 4 - confused 3 - inappropriate 2 - incomprehensible 1 - none
what is the scoring for motor response in the GCS
6 - obeys commands 5 - localises to pain 4 - withdraws from pain 3 - flexion to pain 2 - extension to pain 1 - none
what are flexion and extension to pain also known as and what does this indicate
flexion = decorticate rigidity/posturing
- indicates there may be damage to the cerebral hemispheres, internal capsule, thalamus and potentially midbrain
extension = decerebrate rigidity/posturing
- indicates brainstem damage (below the red-nucleus) damage to the midbrain (worse than decorticate) and damage to the cerebellum
what is transition of flexion to pain (decorticate) to extension to pain (decerebrate) indicative of
uncal (transtentorial) or tonsilar brain herniation
what are the different ways of assessing conscious level
observation (spontaneous movement, seizure like activity)
GCS
brainstem reflexes
Review all other causes of low GCS, temp, BP, HR, cardiovascular, respiratory (O2, CO2), drugs, toxins
*think - could patient be conscious but paralysed?
what are the key brainstem reflexes to loom for in assessing patient consciousness
Pupillary light reactions (CN II+III)
Doll’s eye movement (IV, VI and VIII)
Corneal reflex (V + VII)
If intubated, gentle tugging on endo-tracheal tube
what physiological signs could indicate tectorial herniation of the brainstem (coning)
increasing blood pressure and declining heart rate
what is an eye sign that could indicate raised ICP/uncal herniation
CN third nerve palsy
- ptosis
- dilated pupil
- pupil down and out
what are false localising signs, give examples
signs of raised ICP ipsilateral to pressure
third and sixth nerve palsy
what are true localising sings, give an example
signs of raised ICP contralateral to pressure
hemiparesis
what is an extradural haematoma and where does it most commonly occur
arterial bleeding secondary to trauma
typical from the middle meningeal artery - corresponds to weakest part of the skull (temporal bone)
what are some risk factors for intracranial haematoma
skull fracture
altered consciousness
what are the different types of head injury that can lead to focal neurological sings and/or seizures
diffuse axonal injury
contusion
ICH/IPH
ECH - extradural, subdural
what is the management of a head injury
Stabilise cervical spine
ABC: Airway/Breathing/Circulation
If GCS<8 – intubation + ventilation
Treat raised ICP
Cranial imaging- may need decompressive surgery or removal of haematoma
Neuro observation (GCS)
how is raised ICP treated
Surgery to relieve pressure
heamatoma, ventricular shunt
Osmotic agents e.g. mannitol
Nurse with head at 30-45% (Venous return)
Reduce pain
Maintain good PO2, reduce PCO2
Reduce metabolism (reduce temperature, barbiturates eg thyopentone) - help brain recover
what drugs are NOT useful in treating raised ICP from a bleed
steroids - will work for tumour swelling but not osmotic swelling
how do subdural and extradural haematomas differ on CT
subdural - ellipse shape (curves along edge, think banana)
extradural - lens shape (curves in, almost oval)
how is a subdural haematoma caused
from a head injury causing shearing forces in the bridging veins between the dura and arachnoid
how can subdural haematomas present
can be acute, subacute or chronic
typically delayed symptoms following trauma due to slow venous bleeding
what are the risk factors for subdural haematoma
elderly/dementai/alcoholics - anything causing brain atrophy
aspirin and warfarin
what are the two components of consciousness
- arousal (reticular activating system, pons)
2. awareness of environment (cerebral hemispheres)
what are the decreasing states of consciousness
lethargy
stupurous
obtunded
coma
how does locked in syndrome occur
damage to the brainstem, very commonly the pons
what are the features o flocked in syndrome
patient is fully conscious and aware however they are completely paralysed apart from blinking and vertical eye movement (midline functions so preserved)
- everything below the pons doesn’t work
list some common causes ov a low GCS
Hypoxia / hypercapnia / sepsis / hypotension
Drug intoxication / renal or liver failure
Hypoglycaemia, ketoacidosis
Seizures
Causes of raised intracranial pressure
tumour, stroke, EDH, SDH, SAH, hydrocephalus
