Neurological conditions Flashcards
Stroke: Presentation
Global - loss of consciousness, confusion, agitation
Focal - limb weakness, visual changes, one sided facial droop
General - Headache, paraesthesia, numbness, dysathria, dysphasia, dizziness, vertigo, balance changes.
Stroke: Risk Factors
High blood pressure
Gender
Diabetes Melitus
Physical inactivity
Anticoagulative drugs (haemorrhagic)
High thrombolysis
DVT/PE dislodge
Atrial fibrillation
Alcohol and drug misuse
Stroke: assessment
FAST = Face, Arms, Speech, Time
Fast negative -> MEND test.
Assesses Limbs, Mental status and cranial nerves with key point in each category ( JRCALC)
Differentials
TIA - Strokes last over 24 hours, while symptoms are present it is a STROKE if symptoms resolve it becomes a TIA.
Migraine
Hyperglycaemia
Neurological abnormalities
Trauma
Tumour
Stroke: pathophysiology
- Stroke can be ischaemic or haemorrhagic
- haemorrhagic = blood vessel leakage or rupture causing brain bleed.
- ischaemic = blockage in one of the cerebral blood vessels
- lack of blood supply causes initial ischaemia and eventually infarction
- Location of damage/blockage effects the symptoms shown.
- as Ischaemia and infarction occur quickly, early intervention and recognition are essential to salvage ischaemic tissue.
- thrombosis most common, then embolism, then haemorrhage.
Stroke: Treatment and management
Manage CABCD
O2 if hypoxic
Nil By mouth
Reassurance and explanation
guard against secondary injury (dehydration, hypoxia, hemiparesis)
Assess CBG and correct
12 Lead ECG
IV access
PREALERT AND CONVEY TO STROKE CENTRE with noted onset time as this will dictate treatment
IN hospital - CT scan to identify blockage or bleed, thrombolysis/surgery.
TIA: presentation
Sudden onset, neuro deficit (global or localised)
Confusion, altered LOC, coma
headache
unilateral weakness, paralysis or paraesthesia
Dysarthria (brocas area, speech movement) or dysphasia (wernicke’s area, speech process)
other cranial nerve defecits.
PRESENTATION RESOLVES WITHIN 12-24 hours, normally in minutes.
TIA: risk factors
Hypertension
atrial fibrillation
diabetes
age
gender
Alcohol and drug misuse
Vascular disease
valve disease causing blood pooling and clotting
Atherosclerosis
TIA: pathophysiology
- TIA is a transient episode of neurological dysfunction.
- due to focal brain, spinal cord or retinal ischaemia, neurological impairments which are temporary occur due to brain/nervous cell tissue death/oxygen starvation.
- stroke becomes TIA if signs and symptoms have resolves when assessed by a clinician.
TIA: assessment
FAST, MEND, visual fields - all fully resolved.
ABCD2 (used by some hospitals, only report if used by handover hospital.)
Age (55+) = 1 point
Blood pressure (over 140/90) = 1 point
Clinical features
- unilateral weakness = 2
- speech disturbance = 1
Diabetes = 1 point
Duration of symptoms
- 60 mins+ = 2
-10-59mins = 1
USED TO ASSESS RISK OF STROKE IN FUTURE
TIA: differentials
Migraine
PNES
TIA: treatment and management
Aspirin can be given as not haemorrhagic if symptoms resolve.
REG FLAGS/high risk!
- ABCD2 4+
- prescribed anticoagulants
diagnosed clotting disorders
-diagnosis AF or AF in ECG
-crescendo TIA
TRANSFER TO ED WITH attached stroke unit
No red flags - referral to TIA clinic within 24 hours.
SAH: presentation
thunderclap headache
stiff neck
nausea
photophobia
blurred vision
diplopia
focal defects
confusion
reduced LOC
Symptoms of increased intracranial pressure - increased BP, decreased pulse, altered respiratory patterns.
Prodromal - headache, weakness, dizziness, diplopia, orbital pain.
SAH: risk factors
Hypertension
CAD
AF
Smoking
Drugs/alcohol
Age
Trauma
Tumour
diabetes
Vascular disease
aneurysm
SAH: assessment
Medical emergency requiring rapid assessment and transfer.
ABCD assessment
Disability - check GCS, FAST, PERRL
History of prodromal symptoms
SAH: differentials
Sentinel headache
Stroke
TIA
hypertensive crisis/ acute HTN
SAH: pathophysiology
Intracranial pressure is made up of CSF, brain tissue and blood. Changes in these pressures leads to neurological symptoms.
- Undiagnosed berry aneurysm is often cause of SAH. Aneurysm is caused by hemodynamic stress to cerebral arteries.
- bursting causes bleeding in sub arachnoid space which puts pressure on brain tissue.
- this pressure causes ischaemia and infarction of brain tissue.
- spreading of blood into 4th ventricle and spinal cord cause neck and back pain.
SAH: treatment and management
Maintain ABCD
rapid transport with pre-alert
Actively treat seizures
Pain relief
In-hospital - blood pressure control, medications to reduce ischaemia, surgery
Seizures: Presentation
Focal
- aura
-dependent on location
-muscle jerking
-emotional, LOC changes
Tonic
- Loss of consciousness
- muscle stiffness
- bite on tongue
- trismus
Clonic
- muscle jerking
- loss of bladder control
- Cyanosis if loss of airway
Seizures: risk factors
Epilepsy triggers
- drugs
- alcohol
- stress
- fever
- photophobia
- tiredness
- medication non-compliance
Drugs
excessive alcohol consumption
trauma
tumours
SAH
Stroke
infection
family history
alzheimers
Seizures: Assessment
History of epilepsy
Medication compliance
impact on falling ?
witnessed/unwitnessed
History determines treatment course!!!
AVPU and O2 sats.
Seizures: pathophysiology
- caused by a sudden burst of electrical activity in the brain causing a temporary disruption in the normal message passing between neural cells
- this change in electrical activity can be caused by many triggering factors.
Seizures have a prodromal, Early ictal, ictal and post-ictal phase.
Tonic and clonic meaning
Tonic = rigid, increased TONE
Clonic = rhythmical jerkin
Seizures: Treatment and management
Manage airway, administer O2, avoid crowding.
Resolves in under 5 minutes - no further treatment
Longer than 5 minutes - IV benzodiazepine if access
10 minutes + - 2nd dose
Still convulsing after 10 mins and 2 doses - risk/benefit 3rd dose PREPARE TO VENTILATE
can also give diazepam (rectal) or midazolam (buccal) Consider dignity.
