TLOC, Syncope, NEAD, Epilepsy Flashcards
What is TLOC
Loss of consciousness with an abrupt onset, short duration, spontaneous, complete recovery
Ddx of TLOC
(1. ) Syncope
(2. ) Epileptic seizures
(3. ) NEADs
(4. ) Other: psychiatric conditions = anxiety, panic disorders, Metabolic = hypoglycemia, drug abuse/toxicity
TLOC Ex and Ix
Is it vasovagal or cardiac syncope or epilepsy or NEAD?
- Is there Fx or cardiac disease or sudden death
- Hx: description of event, duration, prodrome? recovery period?
- ECG*** is essential -> Long QT Syndrome, Heart block?
- EEG not usually done unless wanting to determine epilepsy type
- MRI for epilepsy diagnosis
What is Non-epileptic attack disorder NEAD ? Ix + Hx?
(1. ) Loss of consciousness due to psychosocial distress, mental processes. Brain can’t handle a particular memory.
(2. ) More common than epileptic seizure
(3. ) Not caused by abnormal electrical discharges or blood pressure.
Ix and Hx
(5. ) Hx of psychiatric illness, other somatoform disorders
(6. ) Triggers e.g. stress, fear, memories, trauma, PTSD, smells, colours
(7. ) Episode = prolonged atonia, rhythmic pelvic movements, side to side head movements, post ictal crying, eyes closed
(8. ) Duration: 1-20minutes
(9. ) Surprisingly rapid or slow postictal recovery
What is Syncope and presyncope?
(1. ) Syncope, or fainting, is when a person loses consciousness due to reduced cerebral perfusion
(2. ) It usually comes on quickly, doesn’t last long, and there’s usually a spontaneous recovery requiring no resuscitation.
(3. ) Presyncope = light-headedness, muscular weakness, blurred vision, and feeling faint and may lead to syncope
(4. ) Recognising symptoms of presyncope may allow to act fast and prevent evolution of the episode into a full faint.
Three mechanism underlie syncope
(1. ) Cardiac Syncope
- Sudden, light-headedness, palpitations or chest discomfort
- Blackout is brief and recovery is rapid
(2. ) Vasovagal Syncope
- Abnormal ANS causes bradycardia and/or hypotension
- Body overreacts to certain triggers e.g. urination, coughing, prolonged standing, blood.
- Causes drop in HR + BP thus lack of blood flow to brain.
- Pt may experience nausea, malaise, clamminess after event
(3. ) Postural hypotension
- Peripheral vasoconstriction when change from supine to standing position.
- Cause: older age, dehydration, medications/vasoconstricters e.g. CCB, bblockers, ablockers, diuretics and medications that prolong the QT interval like antipsychotics and antiemetics.
Hx, Ex, Ix of Syncope
Pt + witness is important for Dx
(1. )- Hx of heart disease?
- Presyncope or prodromal Sx?
- Triggers?
- Pts appearance - pallor?
- Duration of episode + speed of recovery, in syncope: duration: 5-30s, recovery within 30s
(2. ) Differentiating it against seizures
- Seizures: do not exhibit pallor, abnormal movements, takes >5 mins to recover, often confused
- NEADs: look for emotional triggers, dramatic movement or vocalisation
(3. ) ECG required
(4. ) BP and pulse obtained with pt supine, seated, standing.
(5. ) Auscultation
- pathologic murmurs could suggest structural heart disease.
Mx of Syncope
(1. ) Acute Episode
- Lay in supine position with legs elevated,
- assess vital signs, pulse, respiration, to distinguish cardiac arrest from syncope
(2. ) High risk patients with unexplained syncope
- managed like life threatening syncope
- admitted for management and cardiac monitoring.
(3.) Cardiac syncope: tx of underlying cause
Pathophysiology of Epilepsy
(1.) In epilepsy there is hyper-excitable neuronal activity leading to disturbance of consciousness, motor function, emotion, behaviour, cognition or sensation
(2. ) Seizures develop due to an imbalance between inhibitory and excitatory signals.
- Inhibitory neurons respond to GABA = causes Cl inflow
- Excitatory neurons respond to glutamate = influx of Na and Ca
(3.) The seizure’s clinical features relate to the location and function of the neuronal network that have been recruited into this abnormal synchronous activity.
How is epilepsy classified?
(1. ) Seizure type which is based on area of onset, +/- awareness, associated clinical features
(2. ) Epilepsy type: focal or generalised or both?
What is focal epilepsy? Types? Sx?
(1.) Localised disturbance in one hemisphere leading to focal Sx
Types
(2. ) Simple focal seizure = no LOC
(3. ) Complex focal seizures/Focal Impaired Awareness seizures (FIAS) = LOC present
Focal Sx
(4. ) Occipital onset = lights and blobs of colours
- Temporal lobes = déjà vu
- Sensory involvement = burning, tingling
- Motor involvement = jerking
(5.) Sometimes focal seizure may develop into generalised seizures this is known as ‘Secondary generalised seizure’
What is generalised epilepsy?
- Affects both hemispheres, widespread disturbance of structures and functions. Can include cortical and subcortical structures.
List 5 motor Sx associated with epilepsy
- Tonic (generalised muscle stiffening)
- Clonic (rhythmic muscle jerking)
- Myoclonic (brief, ‘shock-like’ involuntary jerks)
- Atonic (loss of motor tone)
- Spasms (sudden flexion and/or extension movements).
Aetiology of epilepsy (3)
(1. ) Unknown in up to one third of patients.
(2. ) Structural, cortical scarring e.g. Head injury, neuroepithelial tumour, space-occupying lesions, stroke, hippocampal sclerosis, vascular malformation
(3. ) CNS infections
Describe the four stages in epilepsy
(1.) Prodromal = occurs before seizure - confusion, irritability or mood disturbances.
(2. ) Early-ictal = aura - sensory, cognitive, emotional or behaviour changes.
- Not all experience an aura (e.g. generalised seizure onset).
- Aura is suggestive of focal epilepsy and may progress to affect a wider area, or develop into a focal to bilateral tonic-clonic seizure.
(3. ) Ictal
- urinary incontinence, tongue biting, normally lasts 1-2 minutes.
- When seizure lasts >30m, or two seizures occur w/o regaining consciousness after first -> status epilepticus -> medical emergency
(4. ) Post-ictal = recovery period.
- May be altered consciousness, confusion, memory loss, drowsiness or general malaise.
