Chapter 25: Neurology Flashcards
What is a migraine aura due to? (pathophysiology)
Dysfunction of ion channels causing a spreading of cortical depolarisation followed by hyperpoplarisation.
Oestrogen containing pill also sometimes exacerbates migrane
What are the clinical features of migraine?
Prodrome features: malaise, irritability or behaivoural change
20% of people get an aura = often visual e.g. shimmering or silver zig zag lines, sometimes temporary visual field loss
80% dont have an aura
General features:
- severe, throbbing, photophobia, phonophobia and vomiting lasting 4-72hrs
- Worse on movement
- Patients prefer a dark room
What is the management and treatment of migraines?
Avoiding identified triggers e.g. OCP, stress, etc
Acute attack - aspirin, NSAIDs, paracetamol
Nausea - antiemetics (metoclopramide, dompiredone)
Severe attacks - ‘triptans’ e.g. sumatriptan which are potent 5HT seretonin agonists
*overuse may cause medication overuse headache
if attacks are >2 per months, consider prophyalaxis.
1. Beta blockers
2. antidepressants (amitrptyline)
3.anti epileptic drugs (valproate, topiramate)
People with cluster headaches are more often_______ and have higher than average _____ consumption
smokers, alcohol
Clinical features of cluster headaches, how often do they occur, how do they present and location
periodic, lasts about 30-90 mins,
identical beginning at the same time for weeks at a time
May have >1 in 24hr period
might wake up up from sleep
UNILATERAL, periorbital pain
autonomic features: ipsilateral tearing, nasal congestion and conjunctival injection
What is the management and treatment of cluster headaches?
Acute attack = sumpitriptan OR 100% inhaled oxygen
*migraine prohpylaxis is ineffective
Sometimes can be prevented by verapamil, valproate or short course of glucorticoids
3 Possible causes for why trigeminal neuralgia occurs
Irritating lesion at the root of trigeminal root
Compressive lesions
In Multiple sclerosis, can be die to a plaque of demylienation in the brain stem
Characteristics of trigeminal neuralgia ?
UNILATERAL, facial pain
Involves 2/3rd divisions of trigeminal nerve territory
Usually in patients greater than 50 years
What are the clinical features of trigeminal neuralgia? How long does it occur, what is it triggered by, physical signs
Severe Very brief (seconds or less) Triggered by: touch, cold, eating Physical signs: usually absent, but sometimes spasms that make patient wince Can relapse and remit over many years
What is the management of trigeminal neuralgia?
- responds well to carbamazepine
- if patient cant tolerate carbamazepine (try oxycarbazepine, gabapentin, pregabline, amitryptiline or glucorticoids)
- Otherwise surgery
- localised injection of alcohol or phenol into peripheral branch of the nerve
Define epilepsy
abnormal, excessive, synchronous neuronal activity in the brain
Pathophysiology of epilepsy, how does it happen
imbalance between excitatory and inhibitory
- Inhibtory transmitter = GABA which acts on ion channels to increase Cl- influx, and therefore reduce chance of action potential
- Excitatory amino acids, (glutate and aspartate) allow influx of sodium and calcium producing the opposite effect
What are the two main groups of epilepsy and how do they function
- Focal epilepsy: localised distrubance of the cortex, any distrubance of cortical architecture and function can precipitate e.g. tumour, or trauma
Symptoms: according to the cortical area affected
***You can develop generalised seizure after focal
- Generalised epilepsy: spread rapidly, wide distrubance
Name 8 trigger factors for seizures
- sleep deprivation
- Missed doses of epileptic medication
- Alcohol
- Recreational drug use
- Physical and mental exhauston
- Flickering lights including TV or computers
- Metabolic disturbances
- Uncommon: loud noises, music, reading
Focal seizures:
Describe features when seizure is located to :
occipital, frontal, temporal lobes
Occipital: visual change (lights and blobs of colour)
Temporal lobe: False recognition (deja vu), patients often stare blankly, lip smacking or other automatisms such as picking their clothes
Sensory strip = sensory alteration (burning or tingling)
Motor strip= jering
Describe a tonic - clonic (generalised seizure)
- possible initial aura
- Rigidity (tonic) and unconscious falling heavily if standing
(breathing may stop, central cyanosis - Jerking (clonc) because the cortical discharges reduce in frequency
- Flaccid state of deep coma lasting a few minutes
- Post ictal: Confused, disorientated or amnesic
OTHER SIGNS: urinary incontinence, tongue-biting
What sign is pathognomonic of a generalised seizure?
A severely bitten, bleeding tongue after an attack of loss of consciousness
Which drugs can cause a generalised seizure?
Antibiotics: penicillin, isoniazid, metronidazole
Antimalarials
Ciclosporin
Amphetamine/withrawl
What is an absence seizure, when do they start, how often do they occur?
- type of generalised seizure
- ALWAYS start in childhood
- Can occur 20-30times a day (mistaken for daydreaming)
What is a myoclonic seizure, when does it occur more frequently, provoked by?
- Type of generalised seizure
- brief, jerking movement, predominates in the arms
- marked in the morning or when waking up from sleep
- provoked by fatigue, alcohol or sleep deprivation
What is a atonic seizure, when does it occur?
- Type of generalised seizure
- brief loss of muscle tone, resulting in heavy falls with or without loss of consciousness
- occur in the context of epilepsy syndromes
What is a tonic seizure, when does it occur?
Generalised INCREASED in tone
Usually part of epilepsy syndrom
What is a clonic seizure?
Similar to tonic-clonic but not preceding tonic phase.
What are the 4 most common generalised epilepsy syndromes?
- Childhood absence epilepsy
- Juvenile absence epilepsy
- Juvenile myoclonic epilepsy
- GTCS (Generalise Tonic Clonic Seizure) on awakening
