Migrane clinical features, signs and symptoms, diagnosis, treatment

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"Migraine Disorders"[MeSH Terms] AND treatment

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American Headache Society migraine acute preventive treatment guideline diagnosis red flags

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Migraine

Migraine is a recurrent primary headache disorder, usually lasting 4 to 72 hours, with moderate to severe pain and sensory symptoms. It may occur with aura or without aura.

Clinical features: signs and symptoms

A migraine attack can have four phases, although not everyone experiences each one:
  1. Prodrome: Hours to 1-2 days before the headache
    • Fatigue, yawning, mood change, food cravings
    • Poor concentration, neck stiffness, increased urination
  2. Aura: Usually develops gradually and is fully reversible
    • Most commonly visual: flashing lights, zigzag lines, blind spots or scintillating scotoma
    • Sensory: unilateral tingling or numbness that may spread
    • Speech/language disturbance
    • Less commonly, vertigo or motor weakness
      Aura often lasts under an hour and may precede or occur during headache.
  3. Headache phase
    Typical features are:
    • Unilateral, though it can be bilateral
    • Pulsating or throbbing
    • Moderate to severe intensity
    • Worse with routine activity, such as walking or climbing stairs
    • Nausea and/or vomiting
    • Photophobia and phonophobia
    • Possible osmophobia, neck pain, dizziness, impaired thinking, and scalp sensitivity
  4. Postdrome
    • Tiredness, “brain fog,” low mood, difficulty concentrating, or neck discomfort.
Clinical manifestations and criteria summarized from Goldman-Cecil Medicine, p. 3815 and Textbook of Family Medicine, p. 1217.

Diagnosis

Migraine is primarily a clinical diagnosis, based on the headache history and normal neurologic examination.

Migraine without aura: practical diagnostic criteria

At least 5 attacks, each lasting 4-72 hours, with at least 2 of:
  • Unilateral location
  • Pulsating quality
  • Moderate or severe intensity
  • Aggravated by normal physical activity
And during the headache, at least 1 of:
  • Nausea and/or vomiting
  • Photophobia and phonophobia
A headache diary helps document frequency, duration, disability, relation to menstruation, triggers, and use of acute medicines.

Examination

The first assessment should include:
  • Blood pressure and general examination
  • Neck assessment for stiffness
  • Fundus/eye examination when indicated
  • Complete neurologic examination
If the pattern is typical and the neurologic examination is normal, routine CT, MRI, EEG, or lumbar puncture is usually not needed. Textbook of Family Medicine, p. 1217; Goldman-Cecil Medicine, p. 3815.

Red flags: investigate urgently for a secondary headache

Seek urgent medical assessment, particularly for:
  • Sudden maximal headache, “thunderclap” onset
  • New neurologic deficit, confusion, seizure, fainting, or persistent weakness
  • Fever, neck stiffness, rash, or immunosuppression
  • New headache during pregnancy/postpartum
  • Head injury
  • New onset after age 50
  • Cancer, clotting disorder, markedly high blood pressure
  • Papilledema or visual loss
  • A clear progressive change in headache pattern
  • Headache triggered by exertion, sex, coughing, or Valsalva

Treatment

Treatment has two aims: stop an individual attack early and prevent future attacks.

1. Acute treatment

Use treatment early in the attack, ideally when pain is still mild.
Attack severityUsual approach
Mild to moderateAcetaminophen/paracetamol or an NSAID such as ibuprofen, naproxen, aspirin, or diclofenac, if safe for the individual
Nausea/vomitingAdd an antiemetic such as metoclopramide or prochlorperazine, prescribed where appropriate
Moderate to severe or failure of simple analgesiaA triptan such as sumatriptan, rizatriptan, or zolmitriptan, often combined with an NSAID
Cannot use or does not respond to triptansA clinician may consider a CGRP receptor antagonist, such as ubrogepant or rimegepant, or lasmiditan where available
Severe prolonged attack / emergency departmentParenteral antiemetic therapy, NSAID, dihydroergotamine in selected cases, IV fluids if needed, or other protocol-based treatment
Important cautions
  • Triptans should generally be avoided in people with ischemic heart disease, prior stroke/TIA, peripheral vascular disease, or uncontrolled hypertension. They should not be combined with ergot medicines.
  • Avoid opioids and butalbital-containing products for routine migraine care. They have poorer outcomes and increase the risk of dependence and medication-overuse headache.
  • Limit acute medication use to avoid medication-overuse headache. A common practical threshold is avoiding triptans, ergots, opioids, or combination analgesics on 10 or more days/month, and simple analgesics/NSAIDs on 15 or more days/month.
For emergency-department migraine, the recent American Headache Society evidence assessment supports appropriate non-opioid parenteral therapy and specifically advises against hydromorphone; see the AHS emergency update.

2. Preventive treatment

Consider prevention when migraine occurs on roughly 4 or more migraine days per month, is disabling despite good acute therapy, attacks are prolonged, acute medicines are overused, or acute treatments are contraindicated. The American Headache Society prevention guidance also emphasizes disability and impact on daily life, not just attack counts.
Common options, selected according to other conditions and adverse-effect profile:
  • Beta-blockers: propranolol, metoprolol
  • Antiseizure medicines: topiramate, valproate
  • Antidepressants: amitriptyline, venlafaxine
  • CGRP-targeting prevention: erenumab, fremanezumab, galcanezumab, eptinezumab; oral atogepant or rimegepant in suitable settings
  • OnabotulinumtoxinA: for chronic migraine, generally defined as headache on 15 or more days/month for over 3 months, with migraine features on at least 8 days/month
Preventive selection needs clinician review, especially in pregnancy, breastfeeding, cardiovascular disease, liver/kidney disease, depression, asthma, or when taking multiple medicines. Valproate is generally avoided in people who are or may become pregnant because of major fetal risk.

3. Non-drug measures

  • Keep regular sleep, meals, hydration, and exercise routines.
  • Do not skip meals or abruptly change caffeine intake.
  • Identify personal triggers with a headache diary. Common triggers include stress, alcohol, fasting, hormonal fluctuations, sleep disruption, and sensory stimuli, though triggers differ between people.
  • Manage stress with relaxation, CBT, mindfulness, or biofeedback where useful.
  • Treat coexisting anxiety, depression, sleep apnea, or neck pain.
A 2025 evidence-based pharmacologic guideline is indexed on PubMed as PMID 40277319. It supports individualized acute and preventive management; newer evidence may refine choices beyond older textbook regimens.

Ct and mri findings

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"Migraine Disorders"[MeSH Terms] AND "Magnetic Resonance Imaging"[MeSH Terms]

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American Headache Society neuroimaging migraine CT MRI guideline normal neurologic examination

CT and MRI findings in migraine

Typical migraine

  • CT brain is usually normal.
  • MRI brain is usually normal, especially in uncomplicated migraine with a normal neurologic examination.
  • Imaging does not diagnose migraine. Migraine remains a clinical diagnosis based on the history and examination. American Headache Society guidance states that imaging is not indicated for recurrent headaches with migraine features, a normal neurologic examination, and no warning signs.
Goldman-Cecil Medicine, p. 3815.

Possible MRI findings

Some people with migraine, especially migraine with aura or frequent attacks, may show:
  • Small punctate T2/FLAIR hyperintense white-matter foci, often in deep or subcortical white matter
  • Usually nonspecific, nonenhancing, and of uncertain clinical significance
  • These lesions do not by themselves mean multiple sclerosis, stroke, or a brain tumor.
A recent systematic review addresses the association between migraine and white-matter lesions: PMID 41429157. The finding should always be interpreted with the patient’s age, vascular risk factors, symptoms, and lesion distribution.

Imaging during an acute migraine aura

  • CT and conventional MRI are commonly normal.
  • Advanced research imaging can show transient functional or perfusion changes related to cortical spreading depression, but these are not routine clinical findings and are not used to confirm ordinary migraine.

Complicated migraine and important exceptions

Imaging may show abnormalities if the patient has a complication or another diagnosis:
SituationPotential CT/MRI finding
Migrainous infarctionMRI diffusion-weighted imaging shows an acute ischemic infarct, often with a persistent aura/neurologic deficit
Stroke/TIA mimicCT may initially be normal; MRI-DWI and vascular imaging help identify or exclude ischemia
Cerebral venous sinus thrombosisCT venography or MR venography may show venous sinus thrombosis
Subarachnoid hemorrhageNon-contrast CT may show acute blood; CTA and sometimes lumbar puncture are used depending on timing and clinical setting
Tumor, infection, raised intracranial pressure, demyelinationMRI may demonstrate the underlying structural/inflammatory abnormality

When CT or MRI is needed

Neuroimaging is appropriate when there are warning signs such as:
  • Sudden thunderclap onset
  • First or markedly different severe headache
  • Persistent focal weakness, aphasia, confusion, seizure, or reduced consciousness
  • Papilledema or persistent visual loss
  • Fever, neck stiffness, cancer, immunosuppression, or head injury
  • New headache after age 50
  • Pregnancy/postpartum headache
  • Progressive worsening pattern
  • Atypical aura, prolonged aura, or motor weakness
Choice of test
  • Non-contrast CT: preferred first in emergency situations, particularly thunderclap headache, head trauma, or suspected acute hemorrhage.
  • MRI brain: preferred for non-emergency evaluation of atypical, progressive, or focal neurologic presentations because it better detects tumor, infarct, inflammation, posterior fossa lesions, and demyelination.
  • CTA/MRA or CTV/MRV: used if arterial dissection, aneurysm, vascular occlusion, or cerebral venous thrombosis is suspected.
A stable headache pattern that fulfills migraine criteria generally does not require either CT or MRI.

Causes

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American Migraine Foundation migraine causes genetics triggers hormones sleep caffeine

Causes of migraine

Migraine does not usually have one single cause. It is a genetically influenced neurologic disorder in which the brain becomes unusually sensitive to internal and external stimuli. Attacks involve activation of trigeminal pain pathways and release of neuropeptides such as CGRP.

Main contributing factors

  1. Genetic predisposition
    • Migraine commonly runs in families.
    • Common migraine is polygenic, meaning many small genetic effects combine with environmental factors.
    • Rare familial hemiplegic migraine is linked to specific ion-channel gene mutations.
  2. Hormonal changes
    • Menstruation, ovulation, pregnancy/postpartum changes, perimenopause, and hormonal contraceptives can alter attack frequency.
    • This helps explain why migraine is more common in women after puberty.
  3. Brain sensitivity and nervous-system mechanisms
    • Migraine aura is associated with cortical spreading depression, a wave of altered electrical activity across the cerebral cortex.
    • Activation of trigeminal pathways produces throbbing pain, nausea, and light/sound sensitivity.
  4. Individual triggers Triggers do not cause migraine in everyone and may only trigger an attack when the person is already susceptible. Common examples:
    • Stress or emotional upset
    • Poor sleep, excess sleep, shift work, jet lag
    • Skipping meals, fasting, dehydration
    • Alcohol, especially red wine
    • Caffeine excess or caffeine withdrawal
    • Bright/flickering light, loud noise, strong smells
    • Weather or barometric-pressure changes
    • Intense exercise in some people
    • Certain foods in susceptible people, for example aged cheese, processed meats/nitrates, or chocolate
  5. Medication overuse
    • Frequent use of pain medicines can convert episodic migraine into chronic daily headache or medication-overuse headache.
    • Risk is especially high with opioids, butalbital-containing products, combination analgesics, and frequent triptan use.

Important point

A “trigger” is not necessarily the true cause. For example, tiredness, food craving, or neck discomfort may actually be an early prodrome symptom of migraine rather than a trigger.
Keeping a headache diary can identify personal patterns involving sleep, meals, caffeine, menstrual cycle, stress, and medicines. The American Migraine Foundation diet guidance notes that lifestyle and dietary influences often act together rather than a single food being responsible.
Goldman-Cecil Medicine, p. 3815; Bradley and Daroff’s Neurology in Clinical Practice, migraine genetics and triggers sections.
Recent systematic reviews of molecular triggers and vascular responses are indexed as PMID 41923467 and PMID 40790620.

Leptospirosis details explanation

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WHO leptospirosis fact sheet diagnosis treatment clinical guidance

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Leptospirosis

Leptospirosis is a zoonotic bacterial infection caused by spiral-shaped bacteria called Leptospira. It is acquired from the urine of infected animals, especially rats and other rodents, dogs, cattle, pigs, and wild animals.
It is common in tropical, humid, and flood-prone areas, but can occur worldwide.

How it spreads

Humans become infected when contaminated water, mud, or soil contacts:
  • Broken skin, cuts, or abrasions
  • Eyes, nose, or mouth
  • Occasionally by drinking contaminated water
High-risk exposures include:
  • Wading through floodwater
  • Working in rice fields, farms, sewers, or mines
  • Freshwater swimming/adventure sports
  • Contact with rodents or infected animal urine
It is generally not spread from person to person.

Incubation period

Usually 5-14 days, but may range from 2-30 days after exposure. The CDC clinical overview notes that symptoms can be nonspecific and may resemble many febrile illnesses.

Clinical features

The disease has a wide spectrum, from no symptoms or mild flu-like illness to life-threatening multiorgan failure.

1. Mild or anicteric leptospirosis

This is the common form. Symptoms may include:
  • Sudden high fever and chills
  • Severe headache
  • Marked muscle pain, classically in the calves and lower back
  • Weakness and fatigue
  • Nausea, vomiting, abdominal pain, diarrhea
  • Red eyes without pus, called conjunctival suffusion
  • Rash in some patients
  • Cough or sore throat
It may improve after several days. Some patients then develop a second immune phase with recurrent fever, aseptic meningitis, or eye inflammation.

2. Severe leptospirosis: Weil disease

This is a medical emergency and may involve:
  • Jaundice due to liver dysfunction
  • Acute kidney injury, reduced urine output, electrolyte abnormalities
  • Bleeding tendency, petechiae, gastrointestinal bleeding, or pulmonary hemorrhage
  • Low platelet count
  • Severe muscle breakdown
  • Meningitis or encephalopathy
  • Myocarditis or arrhythmia
  • Acute respiratory distress syndrome and respiratory failure
  • Shock and multiorgan failure
The combination of fever, jaundice, acute kidney injury, thrombocytopenia, and recent floodwater/rodent exposure should strongly raise suspicion.

Diagnosis

Diagnosis depends on clinical suspicion plus laboratory confirmation.

Important history

Ask about:
  • Recent flooding or freshwater exposure
  • Rat or rodent exposure
  • Farming, sewage work, animal handling, or outdoor water activities
  • Travel to tropical or endemic regions
  • Fever with calf pain, red eyes, jaundice, or reduced urine output

Tests

TestUse
CBCMay show leukocytosis and thrombocytopenia
Renal function/electrolytesDetects acute kidney injury, hypokalemia or other abnormalities
Liver tests and bilirubinBilirubin can be markedly elevated
UrinalysisProteinuria, hematuria, pyuria, casts
Creatine kinaseMay be elevated due to myositis/rhabdomyolysis
PCR for Leptospira DNAUseful early, using blood/serum; urine may be useful later
IgM antibody testBecomes positive after the first week in many cases
Microscopic agglutination test (MAT)Reference serologic test, often requires paired samples
CSF testingIf meningitis or neurologic manifestations occur
Chest radiograph/CTIf cough, hypoxemia, hemoptysis, or suspected pulmonary hemorrhage
The CDC notes that confirmation can be by detecting Leptospira DNA in blood, serum, urine, or CSF, or by demonstrating an antibody response. The best test depends on the illness duration.

Differential diagnosis

Leptospirosis can resemble:
  • Dengue
  • Malaria
  • Viral hepatitis
  • Influenza or COVID-19
  • Typhoid fever
  • Scrub typhus/rickettsial disease
  • Acute pyelonephritis or sepsis
  • Viral meningitis
  • Hantavirus infection

Treatment

Do not wait for confirmatory tests if clinical suspicion is high, especially in severe disease. Early antibiotics may reduce disease severity and duration.

Mild disease

Typical outpatient therapy, prescribed by a clinician:
  • Doxycycline 100 mg orally twice daily for 7 days for appropriate adults
  • Alternatives may include amoxicillin, ampicillin, azithromycin, or oral penicillin-based regimens depending on pregnancy status, age, allergies, and local guidance
Doxycycline is not suitable for everyone, including many pregnant patients and young children, so treatment must be individualized.

Severe disease or Weil disease

Requires hospitalization and often high-dependency/ICU care:
  • IV penicillin G, ceftriaxone, or cefotaxime, selected according to local protocol and patient factors
  • IV fluids with careful monitoring
  • Management of acute kidney injury and electrolytes
  • Dialysis if indicated
  • Oxygen, ventilation, or ICU support for pulmonary hemorrhage/ARDS
  • Blood products if clinically significant bleeding occurs
A short-lived worsening due to a Jarisch-Herxheimer reaction can occur after antibiotics, with fever, rigors, hypotension, and symptom worsening. This needs observation and supportive care.

Evidence note

Recent systematic reviews, including PMID 38483092 and PMID 38627798, found uncertainty in some antibiotic outcome estimates because available trials have limitations. This does not mean antibiotics should be withheld when leptospirosis is suspected: current public-health guidance still recommends prompt treatment, particularly for significant or severe illness.

Prevention

  • Avoid wading or swimming in potentially contaminated floodwater or freshwater.
  • Wear waterproof boots, gloves, and protective clothing during flood cleanup, sewage work, or farming.
  • Cover cuts with waterproof dressings.
  • Control rodents and safely store food/waste.
  • Do not drink untreated water from potentially contaminated sources.
  • Clean wounds promptly after exposure.
  • Doxycycline prophylaxis is sometimes considered for selected high-risk exposures or travelers, but it is not appropriate for routine self-medication and should follow local public-health or clinician guidance.

Seek urgent care now if

There is fever after floodwater/animal urine exposure plus yellow eyes or skin, reduced urine, shortness of breath, coughing blood, confusion, severe weakness, persistent vomiting, bleeding, or fainting.
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