Neurology Flashcards
Classic explanation of a tension headache
Tight band across the head
Causes of tension type headache
Most common: psychological stress
Others: sleep disturbance, extended periods of mental tension
Typical age of onset of tension headaches
20-30s
Pathophysiology of tension headache
release and activation of inflammatory agents leads to sensitisation of peripheral trigeminal afferents and ultimately in central hypersensitivity
RFs for tension headache
Stress
Missing meals
Sleep disturbance
Mental tension
Clinical presentation of tension headache
generalised head pain frontal or occipital head pain non-pulsatile head pain constricting pain normal neurological examination
Differentials of CHRONIC headache
MMM IT ACHES
MIGRAINE MENINGITIS MEDICATION ICP CHANGE TENSION HEADACHE, TEMP. ART. , TRIGEM. NEURALGIA ARTERIOVENOUS ABNORMALITIES CLUSTER HTN , HAEMORRHAGE EYE (GLAUCOMA) SINUSITIS, SYSTEMIC ILLNESS
Differentials of ACUTE headache
VICIOUS
VASCULAR: haemorrhage, infarction INFECTION / INFLAMM. COMPRESSION: obstructive hydrocephalus, pit. tum. ICP: spont/ intracranial hypoten. OPHTHALMIC: acute glaucoma UNKNOWN: situational factors SYSTEMIC: HTN, CO poisoning
Mx of tension headaches
In the acute patient: simple analgesia
In the chronic patient (>7 episodes per month):
-low dose antidepressant i.e. amitriptyline
-+ non pharmacological relaxation therapies
Key descriptive features of SAH
Sudden onset (thunderclap)
Worst pain ever
Occipital localisation
What is a migraine?
Chronic, genetically determined, episodic disorder presenting with a severe headache causing disability
Epidemiology of migraine
F>M = 2:1
Common condition, more so in the west
Prevalence around 8%
Pathology of migraines
- neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain
- trigeminal neurons release substances that cause dilation of meningeal blood vessels, leakage of plasma proteins into surrounding tissue, and platelet activation
- Sensitises peripheral nerves so that small things like pulsing is considered as pain
- If the headache continues, second- and third-order neurons are sensitised (central sensitisation) and cutaneous stimuli, such as light touch, are interpreted as painful
Migraine RFs
Female Stress Overuse of headache medication \+ FHx Menstruation Obesity Patent Foramen Ovale Lack of sleep
Presentation of migraine
Headache worse with activity Nausea Long term headache Inability to function normally Sensitivity to light
What may come on before a full blown migraine
Aura (changes to vision but no vision loss)
What are some features of prodrome
Yawning
Food cravings
Change to sleep pattern, appetite or mood
Diagnostic criteria for migraine
Aura + headache or
- > 5episodes of headache + n/v + photophobia + >2:
- unilateral
- pulsating
- inability to function
- worse on activity
Triggers of migraine
CHOCOLATE
CHeese OCP (contraceptive pill) Caffeine alcohOL Anxiety Travel Exercise
Mx of migraine
Acute episode
- analgesia + magnesium therapy (sumatriptan)
- NSAID (ketoprofen)
- Rizatriptan
Prophylaxis of migraine
Avoid triggers
- Propanolol + topiramate / amitriptyline
- Valporate, pizotifen, gabapentin
Cluster headache presentation
Rapid onset Pain around one eye Red, watery eye Miosis, ptosis 15min-3hrs duration
Epidemiology of SAH
6-8/100K
Average age of onset 35-65
Causes of SAH
Most commonly rupture of saccular aneurysm (80%)
Arteriovenous malformations account for the rest
