Pathology:                    Pathogenesisunknown – a migraine attack consist of a sequence of phases –

                                                prodromal, aura, headache  andpost-drome.

Classical migraine: Migraine with visual aura

Common migraine: Migraine without visualaura

Hemiplegic migraine: Sporadic or familial –associated with calcium/sodium

channel mutations


Aetiology:                    Mechanismof migraine remains unclear.

Possibly genetic as tends to be more common in patientswith family history.

Triggers: food such as chocolate, cheese etc, exercise,menses, hunger, lack of sleep, stress, combined oral contraceptive pill



Prodromal Phase: Non specific symptoms such as difficultconcentration, irritability, hunger, excessive yawning, tiredness

Aura phase: Visual symptoms such as scintillations,zigzag lines, scotomas; somatosensory symptoms such as parasthesia and dysphasia

Headache Phase: Unilateral throbbing or pulsating andnausea.


Signs:                              ProdromalPhase: Nil

AuraPhase: Weakness,parasthesia and hemiparesis

HeadachePhase: Photophobia,phonophobia


Investigations:          Nilas clinical diagnosis

Consider brain imaging in atypical migraine or in thepresence of red flags


Treatment:                  Acute: Aspirin, Paracetamol, NSAIDs,Anti-emetics, Triptans.

Prophylactic: Beta blockers, Pizotifen,Antiepileptic drugs such as Topiramate and

Sodium Valproate, Amitriptyline andMethysergide



 Idiopathic Intracranial Hypertension


Pathology:                    Idiopathic increase in intracranialpressure with no evidence of an underlying structural brain pathology, althoughthought to be due to inadequate absorption of CSF in the arachnoid villi.


Aetiology:                    Commonly encountered inobese women of child bearing age


Symptoms:                   Headache worse with coughing,sneezing, bending down, visual obscurations (sometimes worse on bending down),pulsatile tinnitus


Signs                              Papilloedema. 6thnerve palsy may also be seen [false localizing sign]


Investigations:          Bloods: FBC, ESR, haemotinics,coagulation and ANA.

                                        Imaging: CT/MRI to excludestructural brain lesions

Special Tests: Lumbar punctureshows an elevated CSF opening pressure

 Humphrey’s visual fields should be performedto assess for defects.


Treatment:                  Conservative: Weightloss

Medical: Lumbar puncture toreduce CSF pressure or Acetazolamide

Surgical: Optic nervefenestration or lumbo-peritoneal shunt procedure


Complications:          Visual loss


Prognosis:                    10% have progressive visualloss an optic atrophy


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