Red Flags signs in secondary headache that suggest intracranial pathology: –

1. New sudden-onset headache reaching maximum intensity within 5 minutes.        
2. New onset headache in a person aged over 50 years.
3. New neurological symptoms such as neurological deficit
4. Systemic symptoms e.g., fever, neck pain/stiffness or photophobia, Dizziness, Vomiting, impaired consciousness, or seizure
5. Contacts with similar symptoms e.g., CO poisoning
6. Immune-compromised illness such as HIV or malignancy
7. Progressive or persistent headache or headache that has changed dramatically.
8. Papilloedema
9. Pregnancy 
10. Precipitating factors such as Valsalva manoeuvre, coughing, sneezing, positional, recent head trauma (in the past 3 months)

Associated features with headache which could indicate serious event such as:

• Fever, impaired consciousness, seizure, neck pain/stiffness or photophobia — consider serious causes such as meningitis and encephalitis.
• Papilloedema — consider space occupying lesions, cerebral venous sinus thrombosis and benign intracranial hypertension.
• New-onset neurological deficit, change in personality and new-onset cognitive dysfunction — consider serious causes such as a cerebrovascular event, malignancy or other space occupying lesions such as subacute or chronic subdural hematoma.
• Atypical aura (duration > 1 hr, or including motor weakness) or aura occurring for the 1^st time in a patient during use of combined oral contraceptives — consider serious causes such as cerebrovascular event.
• Visual disturbance — can be associated with migraine but also with serious causes such as acute closure glaucoma and temporal arteritis.
• Vomiting — can associated with migraine but may also be associated with a serious cause of headache such as mass lesion, brain abscess, or carbon monoxide poisoning.

Cerebral venous sinus thrombosis (CVST)

Risk factors:

Prothrombotic conditions, OCD use, Pregnancy, Malignancy, Infection, Head injury and Inflammatory disease (e.g. SLE, Behçet disease)

Clinical feature:

1. Severe ‎gradual Headache increases over several days and ‎worsens with Valsalva maneuvers & with recumbency. However, some patients with CVST have sudden explosive ‎onset of severe head pain (i.e. thunderclap headache) that mimics subarachnoid hemorrhage.‎
2. The symptoms & signs of CVST can be grouped into three major syndromes:‎
3. Isolated intracranial hypertension syndrome (headache with or without vomiting, ‎papilloedema, and visual problems)‎
4. Focal syndrome (focal deficits e.g. weakness with monoparesis or hemiparesis or aphasia, ‎seizures)‎
5. Encephalopathy (multifocal signs, mental status changes, stupor, or coma)‎
6. Cavernous sinus thrombosis à orbital pain, Reduced visual acuity, Chemosis (conjunctival oedema)‎, Proptosis and Ophthalmoplegia (cranial nerves III to VI)‎

Investigation:

The diagnosis of CVST should be considered in all patients with sub-acute onset headache presenting with a seizure. Contrast enhanced MRI or CT venogram are the imaging modalities of choice.

Treatment:

1. Control of seizures and intracranial hypertension
2. Anticoagulation (heparin or LMWH), followed by long-term anticoagulant

Subarachnoid Haemorrhage

Causes: –

1. Intracranial aneurysm 80% of cases. The majority are located at junction between
   • Anterior communicating artery & Anterior Cerebral artery (Acom/ACA)
   • Distal internal carotid artery & posterior communicating artery junction (ICA/Pcom)
   • Middle cerebral artery bifurcation (MCA).
2. non-aneurysmal peri-mesencephalic SAH: – a distinct pattern of SAH, which is centred on the basal cisterns around the midbrain.
3. Others: arterial dissections, A-V malformation and use of anticoagulants

Risk factors: –

Pseudoxanthoma elasticum / Neurofibromatosis type I	Hypertension	Family history	Smoking
Autosomal dominant polycystic kidney disease	Marfan syndrome	Ehlers-Danlos syndrome	Alcohol / Cocaine use

Clinical feature: –

• ‎due to raised intracranial pressure.‎
• ‎eyelid drooping, diplopia with mydriasis, and orbital pain.‎

Investigation: –

1. Non-contrast CT brain – the presence of the hyperdense appearance of blood in the subarachnoid space/ basal cisterns confirms SAH.
2. A CT head scan performed within 6 hours of symptom onset and reported by a radiologist can rule out a SAH and A lumbar puncture (LP) should not be routinely performed if the CT scan performed within 6 hours is normal. (NICE 2023)
3. The lumbar puncture should be considered if a CT head scan done more than 6 hours after ictus does not confirm the diagnosis of subarachnoid haemorrhage.
4. When a lumbar puncture is indicated, it should be done at least 12 hours after symptom onset, when CSF bilirubin formation (Xanthochromia) is sufficient to be detected reliably.

Complications: –

1. Re-bleeding (in the first 48 hours if not treated) – Consult with a neurosurgeon and arrange an urgent rescan. The neurosurgeon may perform a ventriculostomy to drain the excess cerebrospinal fluid.
2. Acute hydrocephalus – Consult with a neurosurgeon and arrange an urgent rescan. The neurosurgeon may perform a ventriculostomy to drain the excess cerebrospinal fluid.
3. Seizures
4. Vasospasm and delayed cerebral ischaemia – develops between days 3 and 14 after SAH. Suspect the presence of vasospasm/DCI:
   • A drop in GCS score of 2 or more
   • A new focal neurological deficit (e.g., unilateral motor or sensory loss, speech disturbance, or visual field loss) is not attributable to rebleeding, hydrocephalus, hyponatraemia, seizures, or any other cause.
5. SIADH – treat moderate to severe hyponatraemia with hypertonic saline.
6. Neurogenic pulmonary oedema
7. Cardiac complications: –
   • ECG changes: – ST segment/T-wave abnormalities, Prolonged QTc, Arrhythmias and ischaemic changes
   • left ventricular subendocardial injury and takotsubo cardiomyopathy
   • Cardiac arrest

Treatment: –

1. ABCD resuscitation and supportive care. ECG monitoring / BP monitoring via arterial line continuously
2. Give nimodipine (60 mg orally every 4 hours for 14 to 21 days) ASAP after to prevent delayed cerebral ischaemia and improve outcomes.
3. The aneurysm should be secured within 48 hours of onset of symptoms, or within a maximum of 48 hours of diagnosis if presentation was delayed, via endovascular coiling or surgical clipping.
   • Patients with a poor World Federation of Neurosurgical Societies grade/poor neurological function, significant comorbidities, or signs of irreversible brain injury unlikely to make a meaningful neurological recovery are treated conservatively.
4. Stop and where possible reverse all anticoagulation (e.g. warfarin, direct oral anticoagulants). Stop all antiplatelet agents; platelet transfusions are not usually necessary. Do not give antifibrinolytic agents.
5. Maintain systolic blood pressure < 180 mmHg until occlusion of aneurysm.‎
6. Treat moderate to severe hyponatraemia (sodium levels <131 mmol/L) with hypertonic saline ‎‎3%. Hyponatraemia is the most common electrolyte imbalance in SAH.‎
7. Treat seizures using Levetiracetam and sodium valproate. Consult the neurosurgeon
8. VTE prophylaxis – use compression stockings and intermittent compression by pneumatic devices in high-risk patients.

Prognosis: –

The Hunt-Hess Scale is a graded scale used to predict the rate of mortality based solely on the clinical features seen in a patient presenting with an aneurysmal subarachnoid haemorrhage.

Acute angle closure glaucoma

Trigeminal neuralgia

Severe, episodic, unilateral, recurrent facial pain, in the distribution of one or more branches of the trigeminal (5^th) cranial nerve.

Typically, the maxillary or mandibular branches are affected, either alone or in combination.

Involvement of the ophthalmic branch alone is uncommon.

Provoked by light touch to the face, eating, talking, or exposure to cold air.

Risk factors include: multiple sclerosis, advancing age, female sex, family history, hypertension and stroke.

Causes: Mainly idiopathic, other causes include abnormal superior cerebellar

Treatment: –

• Carbamazepine 100 mg BD and titrate every 2 weeks
• If there not suitable then use anticonvulsant e.g., phenytoin.

Giant cell arteritis (or temporal arteritis)

It is a type of chronic vasculitis CC by granulomatous inflammation in the walls of medium and large arteries.

Clinical feature: –

Suspect if the person is aged ≥ 50 years with at least one of:

1. A new onset localised headache that is usually unilateral, in the temporal area, but is occasionally diffuse or bilateral.
2. A temporal artery abnormality, such as tenderness, thickening, or nodularity (45–75% of cases)

Other symptoms and signs suggestive of giant cell arteritis include:‎

1. Systemic features: low grade fever, fatigue, anorexia, weight loss, and depression (occurs in ‎most cases)‎
2. Features of polymyalgia rheumatica: bilateral upper arm stiffness, aching, and tenderness; ‎and pelvic girdle pain (40% of cases)‎
3. Scalp tenderness, especially over the temporal and occipital arteries (50% of cases)‎
4. Intermittent jaw claudication, causing pain in the jaw muscles while eating (nearly 50% of ‎cases)‎
5. Visual disturbances:‎ Permanent partial or complete loss of vision in one or both eyes occurs in up to 20% of cases and is a common early symptom.
6. Neurological features (30% of cases): – Mononeuropathy,  polyneuropathy of arms / legs, TIA or stroke

Investigation: –

1. Blood tests: FBC, LFT, CRP and ESR
2. Temporal artery biopsy

Treatment: –

1. Treat GCA without visual symptoms with prednisolone 40 – 60 mg OD.‎
2. Treat GCA patients with acute or intermittent visual loss with IV methylprednisolone 500 mg – 1 g daily for up to 3 days before commencing ‎oral prednisolone.
3. If there is visual loss (transient or permanent), arrange an urgent assessment by an ophthalmologist.‎
4. Refer all people with suspected GCA for a rheumatologist on the same working day if possible.

Subdural haemorrhage

CT imaging is the first-line investigation and will show a crescentic collection, not limited by suture lines.

Uncommon presentations : – Tentorial SDH or acute parafalcine SDH

An acute SDH is caused by either:‎ Tearing of bridging veins OR bleeding from a damaged cortical artery

There may be a ‘lucid interval’ of a few hours after the injury 

Large acute SDH causes mass effect, midline shift or herniation.

Small or incidental acute subdurals can be observed conservatively.

Surgical options include monitoring of intracranial pressure and decompressive craniectomy.

Extradural Haematoma is due to a fractured temporal or parietal bone damaging ‎the middle meningeal artery or vein, with blood collecting between the ‎dura & the skull.‎

Idiopathic Intracranial Hypertension

It mostly occurs in young obese females in their third or fourth decade.

Female-to-male ratio is between 3:1 to 8:1. There is an increased risk in women with menstrual irregularity.

Clinical feature: –

• Headache tends to be the first symptom: generalised throbbing is worst first thing in the morning and last thing at night. It is relieved on standing (consistent with raised ICP). It is also aggravated by straining, coughing or a change in position.
• Gradual visual field defects; moderate or gross bilateral papilloedema without significant focal intracranial signs
• Six cranial nerve palsy may be found – Double vision due to damage of lateral rectus muscle
• Pulsatile tinnitus

Investigation: –

1. CT or MRI scanning: the ventricles, in contrast to hydrocephalus, are normal or reduced in size
2. Lumbar puncture
3. Bilateral optic disc oedema on fundus examination

Treatment: –

• Acetazolamide is the most effective agent for lowering ICP.
• 1ry headache prophylaxis
• Surgical treatment if all failed – VP shunt

Complication: –

Optic atrophy causing progressive blindness.

Encephalitis

It is inflammation of the brain parenchyma associated with neurological dysfunction.

Causes: –

1. Viral infection (the main cause) à herpes virus is the most common group.
2. Bacterial / fungal / parasitic infection
3. Para-infectious
4. Paraneoplastic (autoimmune) syndromes

Clinical feature: –

• Altered mental status from mild lethargy to profound coma can be seen.‎
• Cognitive behavioural issues – these include: altered personality, withdrawal, inability to make decisions, akinetic mutism, bizarre behaviour, memory problems, and an amnesic state.
• Seizures — complex partial seizures are most commonly seen.‎
• Focal neurological signs (e.g., aphasia, visual disturbances, cranial nerve deficits, lateralised ‎motor weakness, ataxia, tremors, myoclonus, paraplegia, and generalised weakness) are ‎also presenting features.‎
• Signs of meningoencephalitis (e.g., headache, photophobia, neck stiffness) are present in ‎patients with meningeal inflammation.‎
• Symptoms and signs of a systemic illness, such as fever or upper respiratory or ‎gastrointestinal symptoms.‎

Investigation: –

• MRI scanning
• Routine blood, ECG & CXR
• Lumbar puncture – recommended if there is no contraindication, and 2 out of the following 4 symptoms are present: fever, headaches, altered mental status of unknown aetiology, meningism.

Treatment: –

• Supportive care: – airway, circulatory and electrolyte support, DVT-prophylaxis, and GI prophylaxis
• Antiviral treatment +/- Corticosteroids (3 – 5 days): – All cases of suspected community-acquired viral encephalitis are started empirically on Aciclovir (10 mg/kg every 8 hours for at least 14 days) until the cause is determined.
• Initial measures in elevated ICP are elevation of head of bed to 30° to 45°, avoiding compression of the jugular veins, and hyperventilation to a PaCO2 of around 30.
• Subsequently, hyperosmolar therapy with mannitol boluses or hypertonic saline can be used.

Meningitis

Meningococcal septicaemia is infection of the bloodstream by Neisseria meningitidis with subsequent bacterial endotoxin release, and rapid progression to shock and circulatory collapse.

Neisseria meningitidis is a gram-negative, aerobic, encapsulated diplococcus.‎

Neisseria meningitidis is transmitted by aerosol, droplets, or direct contact with secretions ‎from the upper respiratory tract.‎ The incubation period is usually 3 – 5 days.

Neisseria meningitidis capsular group B (MenB) is the most common cause of meningococcal disease in people aged under 25 years.

The most common causative organisms:

1. In neonates (< 1 month of age) → Streptococcus ‎agalactiae, Escherichia coli, Streptococcus pneumoniae, and Listeria ‎monocytogenes are.‎
2. In children aged ≥ 3 months → N. meningitidis, S. pneumoniae, and ‎Haemophilus influenzae b
3. In adults → Streptococcus pneumoniae

Clinical feature: –

• The classic triad of fever, headache, and neck stiffness.
• Changes in mental state are relatively sensitive & occur more often in bacterial than viral meningitis.
• Non-blanching rash is a late sign, it may appear as a: ‎
  • Petechial rash (red or purple non-blanching macules smaller than 2 mm ‎in diameter).  ‎
  • Purpuric (haemorrhagic) rash (spots larger than 2 mm in diameter) ‎
• Kernig’s sign and Brudzinski’s sign
• A suddenly worsening headache, followed by emerging signs of meningism → rupture of a cerebral abscess.

Investigation: –

• CT would be indicated if there are focal neurological signs, papilloedema, controlled or uncontrolled seizures, GCS <12 or diagnostic uncertainty.
  • In children & young people with a reduced or fluctuating level of consciousness (GCS < 9 or a drop of ≥ 3) or with focal neurological signs, perform a CT scan to detect alternative intracranial pathology.
• Perform a lumbar puncture as a primary investigation unless this is contraindicated.
• Submit CSF to the laboratory to hold for PCR testing for N meningitidis and S pneumoniae, but only perform the PCR testing if the CSF culture is negative.

Treatment: –

• Prehospital: Administer a single dose of benzylpenicillin (IV or IM) at the earliest opportunity, but do not delay urgent transfer to hospital.
• Treat suspected meningococcal disease without delay using IV Ceftriaxone 2 g  (Add ‎amoxicillin 2 g if more than 50 years or immunocompromised)‎
• Treat children aged ≥ 3 months with suspected bacterial meningitis ‎without delay using IV ceftriaxone 100 mg/kg.‎
• Treat children younger than 3 months with suspected bacterial meningitis without delay using ‎IV cefotaxime plus either amoxicillin or ampicillin.‎
• Treat children and young people with suspected bacterial meningitis who have recently travelled outside the UK or have had prolonged or multiple exposure to antibiotics (within the past 3 months) with vancomycin in addition to the above antibiotics.
• Give IV dexamethasone, if not given before or with the first dose of antibiotics (0.15 mg/kg, max 10 mg, 4 times daily for 4 days) ‎for suspected or confirmed bacterial meningitis ASAP if LP ‎reveals any of the following:‎
  • Frankly purulent CSF
  • CSF white blood cell count greater than 1000/microlitre
  • Raised CSF white blood cell count with protein concentration greater than 1 g/litre
  • Bacteria on Gram stain.‎
• Anticipate, monitor and correct metabolic disturbances including hypoglycaemia, acidosis, hypokalaemia, hypocalcaemia, hypomagnesaemia, anaemia, coagulopathy.
• Aciclovir if features of encephalitis
• If there are signs of shock, give an immediate fluid bolus (up-to 3 doses) of 20 ml/kg sodium chloride 0.9% over 5 – 10 minutes.

Prophylaxis: –

Give Prophylaxis ASAP (Ciprofloxacin is the recommended 1^st choice chemoprophylaxis) to:

1. People who have had prolonged close contact with the case in a household-type setting during the 7 days before onset of illness (for example, people who are living or sleeping in the same household, pupils in the same dormitory, boy/girlfriends, or university students sharing a kitchen in a hall of residence).
2. People who have had transient close contact with a case only if they have been ‎directly exposed to large particle droplets/secretions from the respiratory tract of a ‎case around the time of admission to hospital.‎
3. Those intubating or suctioning the airways without wearing appropriate PPE