Headaches Flashcards
Primary headache types?
Migraine, tension, cluster, trigeminal neuralgia
Secondary headache types?
Meningitis, encephalitis, haemorrhages (SAH, Subdural and extradural), CNS lesions
Features of tension headache?
Generalised, bilateral, gradual or acute onset. Dul ‘tight band’.
Last 3-4 hours, anaglesics help and moderate severity
RFs for tension headache?
Stree and disturbed sleep
Management for tension headache?
Conservative: headache diaries to avoid triggers and relax.
Medical: simple analgesia (paracetamol, ibuprofen)
MOST COMMON medication-overuse headache (rebund headache)
Migraine definition and potential aetiology?
Chronic condition that causes attacks of headaches potentially via inflammation of the trigeminal nerve changes the way that the brain processes stimuli
Epidemiology of migraines?
RFs?
More common in young adults and 3x more likely female
FHx
Triggers of migraines?
CHOCOLATE Chocolate Hangivers Orgasms Cheese/caffeine OCP Lie-ins Alcohol Travel Exercise
Bright lights, lack of sleep, wine, hormonal changes and stress
Describe migraine headache?
Unilateral, paroxysmal, gradual, pulsating, 4-72hrs, physical activity stress, noise and light exacerbate.
Relieving = lying in dark room and quiet
Associated symptoms of migraine?
Photophobia and phonophobia, Aura: flashing lights. N+V, visual changes and tingling, numbness
Migraine management?
1) Conservative: headache + avoid triggers
2) Acute medical: Paracetamol, ibuprofen and NSAIDs first. if not working then go to triptans
Whats preventative migraine management?
A) propabolol or topiramate.
B) Amitriptyline (antidepressant)
Definition and epidemiology of cluster headache?
RFs?
A neurological disorder characterized by recurrent, severe headaches on one side of head which occur cyclically.
Men and femal 20-40YO
Smoking and alcohol
Pathophysiology of cluster headaches?
Not clear but meant to be hypothalamic activity with secondary trigeminal and autonomic activation.
Presentation of cluster headaches?
UNILATERAL, behind the EYE. Acute onset with CYCLICAL pattern (same time each day). Intense, sharp penetrating pain. 15mins to 3hours and can be triggered by alcohol or strong smells. Can be very severe and disabling
Associated symptoms of cluster headache?
ANS e.g. watery, red eye. Facial flushing and nasal congestion.
Examination: Partial horners (ptosis, miosis).
Pathophysiology of of trigeminal neuralgia?
Facial pain syndrome in the distribution of >1 divisions of trigeminal nerve by compression of nerve by loop of artery or vein.
Associated with MS
Triggers of trigeminal neuralgia?
Touching face, shaving, brushing teeth, eating, talking
Presentation of trigeminal neuralgia?
Unilateral, paroxysmal, lasting for seconds, stabbing or shooting. Numbness is associated and no investigations
What is meningitis and causative organisms?
Inflammation of the meninges.
Bacterial, viruses and TB.
Bacterial: E.coli, group B strep for babies.
Neisseria meningitidis for yound adults.
H.Influenzae, strep pneumoniae for children
Old people = strep pneumoniae, listeria monocytogenes
Viruses: enteroviruses, HSV, VSV, HIV
Meningitis Hx?
Acute and severe.
RFs: Closed communities and crowding. Age <5, >65
Associated symptoms:
Meningism e.g. neck stiffness and photophbia, fever, rash, vomiting and seizures
Examination for Meningitis?
Kernigs sign and Brudzinskis sign. Petechial Rash (non-blanching)
Investigations for meningitis?
CSF is most importatn but ICP is contraindication.
If bacterial: Turbid (cloudy), increased neutrophils (polymorphs), decreased glucose and increased protein
Viral: Clear, increased lymphocytes (mononuclear), normal glucose, normal or increased protein
TB: fibrin web, increased lymphocytes (mononuclear), decreased glucose and increased protein
GP management of Meningitis?
benzypenicillin IM and urgent referral to hospital
A&E management of meningitis?
broad spectrum Abx (ceftriaxone IV, benzypenicillin IM, acyclovir if viral)
Consider IV dexamethasone for targeted Abx
Complications of meningitis?
HEaring loss (common), sepsis, impaired mental state
Encephalitis aetiology viral?
Inflammation of the brain parenchyma.
Usually viral: HSV1-2, CMV, EBV, HIV, measles.
Encephalitis aetiology non-viral?
Non-viral: bacterial meningitis, TB, malaria, listeria, lyme disease, legionella
Epidemiology <1 or >65
Presentation of encephalitis?
Acute onset febrile illness with behavioural, cognitive, psychiatric maniestations
Viral prodrome, fever, headache.
Altered mental state: memory disturbances, personality changes, psychiatric manifestations an impaired consciousness
Investigations of encephalitis?
LP, bloods, EEG, CT/MRI for oedema/hyperintense lesions
Difference between meningitis and encephalitis?
Meningitis is meninges, bacterial, viral, TB and usually impaired consciousness.
Encephalitis is brain parenchyma, usually viral and usually altered consciousness
What aetiology of ICP?
SOL (tumour, abscess, haemorrhage) or hydrocephalus
Presentation of ICP?
Bilateral, gradual, throbbing, worse in morning, coughing and sneezing.
Asssociated are VOMITING, altered GCS and seizures.
Signs of ICP?
Focal neurological symptoms, pappiloedema, Cushings reflex -> triad of Increased SBP, irregular breathing and bradycardia.
Cheyne stokes respiration
Presentation of ICP in children?
Bulging fontanelles, cranial suture separation, increased head circumference, high pitched cry
Investigation of ICP?
Urgent CT head.
Dont do LP as can contribute to brainstem herniation
Features of extradural haemorrhage?
Collection of blood in the potential space between the dura and bone.
HEAD TRAUMA
Young (20-30 male)
Presentation of extradural haemorrhage?
ACUTE following LUCID interval with increasing severe headache.
Decreased GCS due to increased ICP.
Head trauma RF
Investigations for extradural haemorrhage?
Urgent non-contrast CT = LEMON SHAPE
MRI
What happens if bleeding continues from extradural H?
Ipsilateral pupil dilation as compression of outerparasympathetic fibre of oculomotor nerve
Subdural H aetiology?
Collection of blood between dural and arachnoid covering brain.
Rupture of bridging veins (susceptible in elderly and alcoholics from brain atrophy)
These bridging veins drain from cerebral cortex to superior sagittal venous sinus
Presentation of subdural H?
GRADUAL but continuous.
Associated : fluctuationg consciousness, confusion, personality changes and symptoms of Increased ICP
RFs and classification of subdural H?
Head trauma and falls, old age, alcoholics, antcoagulation.
Acute: withing 72 hrs (younger pts, trauma)
Subacute: 3-20 days
Chronic: >3 weeks (headache, confusion)
Subdural H investigations?
Urgent non contrast CT head = BANANA SHAPE
Subdural H management?
Conservative: admit and observe + prophylactic antiepileptics + ICP monitoring + correct coagulopathies
ABCDE and refer to neurology.
if small: observe
if large>10 mm or significant neurological dysfunction = Burr hole or craniotomy
Subarachnoid H aetiology?
Bleeding in subarachnoid space most commonly due to rupture of saccular aneurysm.
SAH presentation?
Occipital (or diffuse), Sudden/thunderclap, ‘worst ever’. Continuous, very severe very quickly.
Associated symptoms and RFs of SAH?
Meningism and Raised ICP symptoms.
Polycystic kidney disease, alcohol, smoking and HTN
Investigation for SAH?
Urgent non-contrast CT scan <12hours. Sensitivity decreases with time
LP: if CT normal. Xanthochromia or oxyhaemoglobin. From 12 hours of symptom onset. Xanthochromia done via photospectroscopy
CNS tumour definition?
Primary brain tumours arising from any of the brain tissue types> Most are from glial cells *supportuve of NS). Meningiomas fro, arachnoid cells
Most common paediatric brain tumour?
Medulloblastoma and gliomas
CNS tumour presentation?
Headache: bilateral, gradual, throbbing, worse in morning and coughing sneezing. = ALL DUE TO ICP.
FLAWS
Focal neurological signs, weakness, difficulty walking, seizures, personality changes
Examples of focal neurological symptoms?
Dysphagia, hemiparesis, ataxia, visual field defects, cognitive impairment
RFs for CNS tumour?
Cancer Hx and FHx.
Ionising radiation
Immunosppression
Inherited conditions e.g. neurofibromatosis
Frontal lobe tumour presentation?
personality disturbance, apathy, impaired intellect
R parietal lobe tumour presentation?
L homonymous hemianopia, L sided hemiparesis and sensor loss
Vestibular schwannoma presentation?
Progressive deafness
CNS tumour investigations?
CT, MRI
CXR< CT Thorax, AXR,
Biopsy
Headache red flags?
SPOON Systemic signs or symptoms Neurological signs or symptoms Onset Older >50 new headache Progression of existing headache
