By the end of this note you will be able to take a focused history, perform a targeted examination, recognise red‑flag features, and outline an initial investigation and management plan for common and serious headaches seen in Kenyan clinical rotations. Always verify drug choices, doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
A headache is a pain or discomfort localized to any region of the head, scalp, or neck, with or without associated symptoms (nausea, photophobia, phonophobia). Red‑flag headaches are those that suggest an underlying secondary, potentially life‑threatening disorder and warrant urgent evaluation.
Anatomy and physiology you need
| Structure | Relevance to headache |
|---|---|
| Meninges (dura, arachnoid, pia) | Stretch or inflammation → meningeal pain |
| Cerebral arteries & veins | Vascular dilation or thrombosis → pulsatile or ischemic pain |
| Trigeminal nerve (V) | Primary afferent pathway for most primary headaches |
| Cervical nerves (C1‑C3) | Referred pain from neck → tension‑type headache |
| Brain parenchyma | Intracranial mass or edema → raised ICP headache |
| Autonomic nuclei (hypothalamus) | Cluster headache, migraine aura |
Causes and risk factors
| Category | Common conditions in Kenya | Key risk factors |
|---|---|---|
| Primary | Migraine, tension‑type, cluster | Family history, stress, hormonal changes |
| Infectious | Cerebral malaria, tuberculous meningitis, cryptococcal meningitis, HIV‑related opportunistic infections | Recent travel, immunosuppression, poor malaria prophylaxis |
| Vascular | Subarachnoid haemorrhage, hypertensive encephalopathy, cerebral venous sinus thrombosis | Uncontrolled hypertension, pregnancy, dehydration |
| Structural | Brain tumour, abscess, hydrocephalus | HIV (primary CNS lymphoma), TB (tuberculoma), sickle cell disease (stroke) |
| Metabolic / systemic | Severe anaemia, electrolyte imbalance, sickle cell crisis, rheumatic fever (post‑streptococcal) | Sickle cell disease, chronic kidney disease, malnutrition |
| Trauma | Post‑concussive headache, intracranial bleed | Road‑traffic accidents, falls |
Pathophysiology
- Primary headache → trigeminovascular activation → release of CGRP, substance P → vasodilation & neurogenic inflammation → pain perception
- Migraine aura → cortical spreading depression → transient neuronal depolarisation → visual/ sensory symptoms → subsequent trigeminal activation
- Tension‑type → peripheral myofascial nociception → central sensitisation → bilateral pressing pain
- Subarachnoid haemorrhage → blood in CSF → meningeal irritation + sudden rise in ICP → thunderclap headache
- Tuberculous meningitis → Mycobacterium TB infection of meninges → exudate → basal meningeal inflammation → headache, cranial nerve palsies
- Cerebral malaria → sequestration of parasitized erythrocytes → microvascular obstruction → cerebral edema → diffuse headache
- Cerebral venous sinus thrombosis → thrombus → impaired venous outflow → raised ICP → headache often worse when supine
Each step links a precipitating event to the clinical manifestation of headache.
Clinical features
| Aspect | Key questions / findings | Why it matters |
|---|---|---|
| Onset | Sudden (“thunderclap”) vs gradual; first attack vs recurrent | Sudden onset suggests subarachnoid haemorrhage or vascular event; gradual points to primary headache or infection |
| Location | Unilateral, bilateral, frontal, occipital, cervical | Unilateral piercing pain → trigeminal autonomic cephalgias; occipital pain → cervicogenic or posterior fossa lesion |
| Quality | Throbbing, pressure‑like, stabbing, burning | Throbbing typical of migraine; stabbing suggests cluster or trigeminal neuralgia; burning may indicate neuropathic pain |
| Duration | Seconds, minutes, hours, days, chronic (>15 days/month) | Short bursts → primary stabbing headache; >15 days/month → chronic migraine or medication‑overuse |
| Pattern | Episodic vs continuous; seasonal variation | Episodic with triggers → primary; continuous worsening → secondary cause |
| Triggers | Light, noise, foods, alcohol, stress, hormonal changes, posture, travel, dehydration | Identifies migraine or tension‑type triggers; posture‑related pain may point to intracranial mass or meningitis |
| Associated symptoms | Nausea/vomiting, photophobia, phonophobia, aura, fever, neck stiffness, focal neurological deficits, seizures, visual loss, diplopia, altered mental status | Photophobia/phonophobia → migraine; fever/neck stiffness → meningitis; focal deficits → stroke, tumour, HIV‑related opportunistic infection |
| Red‑flag history | Age >50 new onset, immunosuppression (HIV, steroids), recent trauma, cancer, TB exposure, sickle‑cell crisis, malaria, rheumatic disease, anticoagulant use, progressive worsening, morning headache, vomiting >2 times, weight loss | Each flag raises suspicion for secondary, potentially life‑threatening causes that need urgent work‑up |
| Medication use | Acute analgesics, triptans, NSAIDs, opioids, over‑the‑counter combinations, prophylactic agents | Over‑use can cause medication‑overuse headache; lack of response may suggest secondary cause |
| Social / occupational | Work stress, shift patterns, exposure to chemicals, travel to endemic areas | May uncover occupational headache or exposure‑related infections (e.g., malaria, TB) |
Examination findings
| Finding | Expected abnormality | Rationale |
|---|---|---|
| General appearance | Fever, pallor, jaundice, cachexia | Systemic infection (TB, malaria), anemia (sickle cell), HIV‑related wasting |
| Vital signs | Hypertension, fever, tachycardia, low GCS | Hypertensive crisis can cause headache; fever → infection; low GCS → raised ICP or encephalitis |
| Head | Scalp tenderness, sinus tenderness, temporal artery thickening | Temporal arteritis (elderly); sinusitis; meningitis (neck stiffness) |
| Neck | Nuchal rigidity, Kernig/Brudzinski signs | Meningeal irritation from meningitis, TB meningitis, subarachnoid haemorrhage |
| Cranial nerves | Visual field cuts, papilledema, diplopia, facial weakness | Papilledema = raised ICP; cranial nerve palsies = cavernous sinus thrombosis, HIV‑related lesions |
| Motor & sensory | Weakness, sensory loss, ataxia | Focal deficits indicate stroke, space‑occupying lesion, HIV opportunistic infection |
| Coordination & gait | Dysmetria, gait instability | Posterior fossa pathology, cerebellar involvement (malaria cerebral, TB) |
| Fundoscopy | Papilledema, optic disc pallor, retinal hemorrhages | Raised ICP, optic neuritis (HIV), malaria retinopathy |
| Skin | Rash, petechiae, purpura, livedo | Vasculitis (HIV, rheumatic disease), meningococcal sepsis, sickle‑cell vaso‑occlusion |
| Neck veins | Jugular venous distension | Cerebral venous sinus thrombosis (pro‑thrombotic states in HIV, sickle cell) |
Differential diagnosis
| Condition | Points toward it | Distinguishing feature |
|---|---|---|
| Primary migraine | Aura, throbbing, photophobia, family history | Normal neuro exam, no red flags |
| Tension‑type headache | Bilateral pressure, stress‑related, no nausea | Absence of photophobia, normal exam |
| Cluster headache | Unilateral orbital pain, lacrimation, nasal congestion, episodic | Autonomic signs, attacks at night |
| Temporal arteritis | Age >50, scalp tenderness, jaw claudication, ESR ↑ | Temporal artery thickening, visual loss |
| Subarachnoid haemorrhage | Thunderclap onset, neck stiffness, loss of consciousness | CT within 6 h positive, xanthochromia in CSF |
| Bacterial meningitis | Fever, neck stiffness, altered mental status | CSF neutrophils, low glucose |
| Tuberculous meningitis | Subacute onset, weight loss, HIV+, basal meningeal enhancement | CSF lymphocytes, high protein, low glucose |
| Cerebral malaria | Recent travel to endemic area, fever, seizures, coma | Peripheral smear positive for Plasmodium falciparum |
| HIV‑related opportunistic infection (e.g., cryptococcal meningitis) | HIV+, CD4 <100, chronic headache, papilledema | CSF India‑ink positive, low opening pressure |
| Cerebral venous sinus thrombosis | Pro‑thrombotic state (sickle cell, HIV), headache worsening, seizures | MRV shows venous occlusion |
| Space‑occupying lesion (tumour, abscess) | Progressive headache, focal deficits, seizures, HIV+ | Imaging shows mass effect |
| Medication‑overuse headache | Frequent analgesic use, daily headache | Improves after withdrawal of medication |
| Hypertensive encephalopathy | Severe hypertension, visual changes, papilledema | BP markedly elevated, reversible with BP control |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Non‑contrast CT head | Acute bleed, mass effect, hydrocephalus | Hyperdense bleed → SAH; hypodense lesion → tumour/abscess |
| MRI brain with contrast | Detailed parenchymal pathology, meningitis, venous thrombosis | Enhancing leptomeninges → meningitis; venous sinus loss → thrombosis |
| Lumbar puncture (CSF analysis) | Infection, subarachnoid bleed, inflammatory disease | Neutrophils + low glucose → bacterial meningitis; lymphocytes + low glucose → TB meningitis; xanthochromia → SAH |
| CSF PCR panel | Specific pathogens (HSV, VZV, CMV, TB) | Positive PCR confirms viral or TB aetiology |
| Full blood count & peripheral smear | Anemia, malaria parasites, sickle cell crisis | Parasites present → malaria; sickled cells → sickle cell |
| ESR / CRP | Inflammation, temporal arteritis, infection | ESR >50 mm/h in >50 yr suggests arteritis |
| HIV test + CD4 count | Immunosuppression status | CD4 <200 → high risk for opportunistic CNS infections |
| Serum electrolytes & renal function | Metabolic causes, drug toxicity | Hyponatraemia → SIADH, renal failure → uremic encephalopathy |
| Blood cultures | Bacterial sepsis, meningococcal disease | Growth of pathogen guides antibiotics |
| Coagulation profile | Bleeding risk, thrombosis work‑up | Elevated INR → anticoagulant effect; D‑dimer ↑ may prompt MRV |
| Fundoscopy (direct) | Papilledema, optic disc changes | Papilledema → raised ICP; disc pallor → optic neuritis |
| Temporal artery ultrasound (if arteritis suspected) | Vessel inflammation | Halo sign → temporal arteritis |
Diagnosis and severity
- Classify the headache
Primary – migraine, tension‑type, cluster – when red flags absent, neuro exam normal, and investigations unrevealing.
Secondary – any headache with one or more red flags, abnormal exam, or positive investigations.
- Determine severity (use a simple three‑tier system)
| Tier | Clinical picture | Management focus |
|---|---|---|
| Mild | Intermittent, tolerable, no functional limitation, no red flags | Outpatient education, lifestyle modification, acute abortive therapy, consider prophylaxis if frequent |
| Moderate | Daily or disabling pain, limited activities, but no neurological deficit or systemic danger | Prompt outpatient work‑up, start appropriate acute therapy, begin prophylaxis, arrange follow‑up within 1 week |
| Severe / urgent | Sudden thunderclap, progressive worsening, focal deficits, altered consciousness, papilledema, systemic signs (fever, hypertension) | Immediate emergency evaluation, neuro‑imaging, possible lumbar puncture, admission, targeted disease‑specific treatment (e.g., antibiotics for meningitis, antiretroviral optimisation, antimalarial therapy, anticoagulation for CVST) |
- Assign a working diagnosis based on the most likely condition after history, exam, and initial investigations. Document the rationale, any pending tests, and the plan for definitive confirmation.
- Safety monitoring
Vital signs every 15 min initially for severe cases, then hourly.
Neurological status (GCS, pupil size, motor strength) at each assessment.
ICP signs – watch for worsening headache, vomiting, decreasing consciousness.
Treatment response – reassess pain score, side‑effects, and any new deficits within 2 hours of therapy initiation.
- Escalation criteria – development of new focal deficit, worsening consciousness, persistent vomiting, or failure of initial therapy within 24 hours mandates reassessment, repeat imaging, and possible transfer to a higher‑level centre.
By systematically applying the history, focused examination, targeted investigations, and severity grading, clinicians can rapidly differentiate benign primary headaches from life‑threatening secondary causes common in the Kenyan setting, ensuring timely, appropriate treatment and safe patient outcomes.
Management
Immediate stabilisation
| Situation | Action | Rationale |
|---|---|---|
| Sudden severe (“thunderclap”) headache ± neck stiffness | Secure airway, give high‑flow O₂, obtain IV access, start IV antihypertensive if MAP > 110 mmHg, give IV mannitol/ hypertonic saline if raised ICP suspected, arrange emergent CT head | Prevent secondary brain injury and treat possible subarachnoid haemorrhage or cerebral venous thrombosis |
| Fever, neck rigidity, altered mental state | Same as above + give broad‑spectrum IV antibiotics (e.g., a third‑generation cephalosporin + vancomycin) after cultures, start antitubercular therapy if TB meningitis likely | Covers bacterial meningitis while awaiting CSF results |
| Focal neurological deficit or seizures | Give IV benzodiazepine for seizure control, start antiepileptic loading dose, protect airway, consider IV steroids if tumour/abscess suspected | Stops ongoing neuronal injury |
Definitive treatment
- Primary headache (migraine, tension‑type, cluster)
- Migraine – acute: triptan class, anti‑emetic, NSAID; preventive: beta‑blocker, calcium‑channel blocker, antiepileptic.
- Tension‑type – simple analgesic, muscle relaxant, stress‑management.
- Cluster – high‑flow O₂, sub‑cutaneous sumatriptan, preventive verapamil.
- Secondary headache – treat underlying cause:
- Subarachnoid haemorrhage – neurosurgical clipping/endovascular coiling, nimodipine to prevent vasospasm.
- Cerebral venous sinus thrombosis – therapeutic anticoagulation (LMWH → warfarin).
- Meningitis – pathogen‑directed antibiotics; adjunctive dexamethasone for bacterial meningitis.
- Tuberculous meningitis – intensive phase antitubercular drugs + adjunctive steroids.
- HIV‑related opportunistic CNS infection – appropriate antiretroviral optimisation and targeted antimicrobial therapy.
- Malaria cerebral – parenteral artesunate, manage raised ICP.
- Sickle cell vaso‑occlusive crisis with headache – adequate hydration, analgesia, blood transfusion if indicated.
Monitoring & follow‑up
- Vital signs, neurological status (GCS, pupil size, motor power) q1‑2 h in ICU, then q4 h on ward.
- Repeat imaging if neurological picture worsens.
- Laboratory trends (CBC, electrolytes, renal & liver function, inflammatory markers).
- Outpatient review within 1–2 weeks for primary headache; earlier if secondary cause treated.
Contra‑indications & safety
- Triptans: avoid in uncontrolled hypertension, ischemic heart disease, cerebrovascular disease.
- NSAIDs: avoid in renal failure, active peptic ulcer, severe asthma.
- Anticoagulation: contraindicated in active intracranial bleed or recent major surgery.
- Steroids: use cautiously in uncontrolled diabetes, active infection without coverage.
Complications and prognosis
| Complication | Typical outcome if untreated | Preventive/early‑treatment measure |
|---|---|---|
| Subarachnoid haemorrhage → re‑bleed, vasospasm, permanent deficit | High mortality/morbidity | Early aneurysm securing, nimodipine, BP control |
| Cerebral venous thrombosis → venous infarction, seizures | Variable; can be fatal | Prompt anticoagulation |
| Bacterial meningitis → hydrocephalus, hearing loss, seizures | Significant morbidity | Immediate antibiotics + steroids |
| TB meningitis → basal meningitis, infarcts | Poor neurological recovery | Early antitubercular therapy + steroids |
| Chronic migraine → medication‑overuse headache, disability | Reduced quality of life | Structured preventive regimen |
| HIV CNS opportunistic infection → neurocognitive decline | Progressive deterioration | ART optimisation, pathogen‑specific therapy |
Overall, prognosis hinges on rapid identification of red‑flags and timely definitive therapy. Primary headaches have an excellent long‑term outlook with appropriate prophylaxis.
High‑yield exam points
- Red‑flag checklist (“SNOOP” plus local additions): Sudden onset, Neurological deficit, Onset < 50 y or > 70 y, Older patient with new headache, Prior headache history change, Systemic signs (fever, weight loss, HIV, TB), Occupational exposure, Pregnancy/post‑partum.
- Thunderclap headache → always image (CT ± LP) before assuming migraine.
- Meningitis vs. TB meningitis – CSF glucose < 40 % of serum, lymphocytic predominance, high protein suggest TB; neutrophils, very low glucose suggest bacterial.
- Cerebral venous sinus thrombosis often presents with headache + papilledema + focal signs; MRV is diagnostic.
- Common wrong first step: prescribing triptans for a thunderclap headache without imaging.
- Examiner bedside question: “What red‑flag would make you order an urgent CT in a 30‑year‑old woman with a 2‑day history of worsening frontal headache?” – answer: sudden onset, papilledema, focal deficit, immunosuppression, etc.
Clinical case
Case: 28‑year‑old HIV‑positive female (CD4 = 180 cells/µL) presents with a 12‑hour history of severe, diffuse headache, photophobia, neck stiffness, and low‑grade fever. No focal deficits. Fundoscopy shows papilledema.
Questions
- What is the most urgent investigation?
Answer: Non‑contrast CT head followed by lumbar puncture if CT is normal.
- Which empirical therapy should be started now?
Answer: Broad‑spectrum IV antibiotics covering common bacterial meningitis pathogens (e.g., third‑generation cephalosporin + vancomycin) plus adjunctive dexamethasone; consider adding antitubercular drugs if TB meningitis is high on the list.
- What finding on CSF would shift management toward TB meningitis?
Answer: Lymphocytic predominance, markedly elevated protein, low glucose (< 40 % of serum) and positive acid‑fast bacilli or PCR for Mycobacterium tuberculosis.
Practice questions
Question 1
A 45‑year‑old man with uncontrolled hypertension presents with a sudden “worst ever” headache, vomiting, and a brief loss of consciousness. Neurological exam shows neck rigidity but no focal deficit. What is the next best step?
A. Give oral ibuprofen and discharge
B. Immediate non‑contrast CT head
C. Start oral triptan therapy
D. Perform lumbar puncture at bedside
Answer: B. Immediate non‑contrast CT head
Explanation: Sudden severe headache with meningeal signs mandates emergent imaging to rule out subarachnoid haemorrhage before LP.
Question 2
A 22‑year‑old university student complains of a 3‑day history of unilateral throbbing pain, lacrimation, and nasal congestion. No fever or neurological signs. Which preventive medication is most appropriate?
A. Beta‑blocker
B. Calcium‑channel blocker
C. Antidepressant
D. Antiepileptic
Answer: B. Calcium‑channel blocker
Explanation: Verapamil is first‑line prophylaxis for cluster headache, matching the autonomic features described.
Question 3
A 35‑year‑old woman with sickle cell disease presents with a diffuse headache, fever, and a new focal motor deficit. MRI shows a left parietal infarct. Which treatment is indicated?
A. High‑dose aspirin only
B. Therapeutic anticoagulation
C. Immediate lumbar puncture
D. Intravenous mannitol
Answer: B. Therapeutic anticoagulation
Explanation: In sickle cell patients, cerebral venous sinus thrombosis can present with infarct and headache; anticoagulation is the mainstay.
Question 4
A patient on chronic NSAIDs for tension‑type headache develops new onset vomiting, confusion, and papilledema. Which condition should be high on the differential?
A. Medication‑overuse headache
B. Intracranial tumour causing raised ICP
C. Migraine with aura
D. Sinusitis
Answer: B. Intracranial tumour causing raised ICP
Explanation: Papilledema and altered mental status indicate raised intracranial pressure, prompting imaging for mass lesion.
Question 5
A 60‑year‑old farmer with a history of malaria presents with a dull, bilateral headache, low‑grade fever, and mild neck stiffness. CSF shows 150 cells/µL (predominantly lymphocytes), protein 120 mg/dL, glucose 55 % of serum. What is the most likely diagnosis?
A. Bacterial meningitis
B. Cerebral malaria
C. Tuberculous meningitis
D. Viral meningitis
Answer: D. Viral meningitis
Explanation: Lymphocytic pleocytosis with relatively preserved glucose points to viral aetiology; TB would have lower glucose and higher protein.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.