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CNS History Viva - Head and Neck Symptoms
Headache Viva: Questions & Answers for MD General Medicine Exams
I. Basic Concepts & Classification
Q1: What are the most common types of primary headaches you encounter in clinical practice?
A1: The most common primary headaches are Tension-Type Headache (TTH), Migraine (with or without aura), and Cluster Headache.
Q2: How do you broadly classify headaches? What's the fundamental difference between primary and secondary headaches?
A2: Headaches are broadly classified into primary and secondary types.
Primary headaches are standalone conditions where the headache is the disorder itself, not a symptom of another underlying condition (e.g., migraine, TTH, cluster).
Secondary headaches are symptoms of an underlying, identifiable structural or systemic disease (e.g., headaches due to brain tumors, meningitis, stroke, or severe hypertension).
Q3: Can you explain the key diagnostic criteria for Migraine without Aura according to ICHD-3?
A3: According to ICHD-3(International Classsification of Headache Disorders),
Migraine without Aura requires: At least 5 attacks fulfilling following criteria
Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated).
Headache has at least two of the following four characteristics:
Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by or causing avoidance of routine physical activity (e.g., walking, climbing stairs)
During the headache, at least one of the following:
Nausea and/or vomiting
Photophobia (aversion to light) and phonophobia (aversion to sound)
Not better accounted for by another ICHD-3 diagnosis.
Q4: Differentiate between tension-type headache and migraine
Tension-Type Headache (TTH): Typically bilateral, pressing/tightening (non-pulsating) quality, mild-to-moderate intensity, not aggravated by routine physical activity. May have photophobia or phonophobia, but not both, and no nausea/vomiting.
Migraine: Typically unilateral (though can be bilateral), pulsating/throbbing quality, moderate-to-severe intensity, aggravated by routine physical activity. Characteristically associated with nausea/vomiting and/or photophobia and phonophobia.
Q5: What defines a "thunderclap headache," and why is it considered a medical emergency?
A5: A thunderclap headache is a sudden-onset, severe headache that reaches its maximum intensity within less than one minute. It's considered a medical emergency because it can be the presenting symptom of life-threatening conditions such as Subarachnoid Hemorrhage (SAH), Cerebral Venous Thrombosis (CVT), Cervical Artery Dissection, or Reversible Cerebral Vasoconstriction Syndrome (RCVS). Immediate investigation is crucial.
II. History Taking & Red Flags
Q1: You have a patient presenting with headache. Walk me through your systematic approach to taking a headache history. What are the absolute essential questions you must ask?
A1: My systematic approach would follow a structured format:
Onset: When did it start? Was it sudden (thunderclap), subacute, or chronic?
Duration & Frequency: How long does each episode last? How often do they occur? Is it constant or intermittent?
Character: What does the pain feel like (pulsating, dull, stabbing, tight)?
Location & Radiation: Where is the pain located? Does it spread?
Severity: On a scale of 0-10, how severe is it? How does it affect daily activities?
Associated Symptoms: Nausea, vomiting, photophobia, phonophobia, aura, fever, neck stiffness, neurological deficits (weakness, numbness, speech/visual changes), autonomic symptoms (for cluster).
Aggravating/Relieving Factors: What makes it worse/better? (e.g., physical activity, rest, light, sound, medications).
Past History of Headaches: Any similar headaches before? Previous diagnosis, investigations, treatments?
Medication History: Any regular painkiller use (MOH risk)? Other relevant medications (e.g., OCPs, anticoagulants)?
Red Flags: Specifically ask about any new neurological symptoms, fever, visual changes, new onset in older age, worsening pattern, or thunderclap onset.
Q2: List the "red flags" in headache. Why is each one a red flag?
A2: SNOOP10 mnemonic:
Systemic symptoms (fever, weight loss, malignancy, HIV): Suggests infection (meningitis, encephalitis), systemic inflammatory disease, or cancer.
Neurological symptoms or signs (papilledema, focal deficits, altered consciousness, seizures): Points to structural brain pathology (tumor, stroke, abscess, increased ICP).
Onset is sudden and maximal at onset (Thunderclap): High suspicion for SAH, cerebral venous thrombosis, arterial dissection.
Older patient (new headache >50 years): Increased risk of Giant Cell Arteritis, mass lesions, chronic subdural hematoma.
Pattern change or new headache (worsening, change in character/frequency): Suggests a progressive underlying lesion like a tumor, or chronic subdural.
Precipitated by Valsalva, cough, exertion: Can indicate increased ICP, Chiari malformation, or other structural lesions.
Progressively worsening: Similar to pattern change, indicative of an expanding lesion.
Pregnancy or postpartum: Increased risk of cerebral venous thrombosis, pre-eclampsia, pituitary apoplexy.
Painful eye with autonomic features: Could suggest acute glaucoma, or other causes beyond primary headache.
Papilledema: Direct sign of raised intracranial pressure.
Position related (e.g., worse with standing - CSF leak; worse lying down - high ICP).
Previous headache history but the current headache is different or "worst ever".
Q3: A 60-year-old patient presents with a new onset, daily headache. What specific questions would you ask to rule out Giant Cell Arteritis (GCA)?
A3: For a 60-year-old with new daily headache, GCA is a critical consideration. I would specifically ask about:
Temporal region pain: Is the pain localized to the temples? Is it tender to touch?
Jaw claudication: Pain or fatigue in the jaw while chewing.
Visual symptoms: Any transient or permanent vision loss (amaurosis fugax), double vision (diplopia), or blurred vision?
Scalp tenderness: Pain when brushing hair or resting head on a pillow.
Constitutional symptoms: Fever, malaise, unexplained weight loss, night sweats.
Limb claudication: Pain in arms or legs with exercise due to large vessel involvement.
Q4: Describe the key features you'd look for in a history suggestive of a Subarachnoid Hemorrhage (SAH).
A4: Key features pointing to SAH include:
Thunderclap headache: Sudden onset, reaching maximum severity in seconds to minutes ("worst headache of life").
Associated symptoms: Nausea, vomiting, neck stiffness (meningismus), photophobia, transient loss of consciousness, or seizures.
Absence of prior similar headaches (though a history of "sentinel headaches" can precede a major SAH).
Recent strenuous activity or Valsalva maneuver as a trigger.
Q5: What is Medication Overuse Headache (MOH)? How do you identify it from the history?
A5: Medication Overuse Headache (MOH) is a secondary headache caused by the chronic overuse of acute headache medications. It occurs when patients take acute headache treatments too frequently, leading to a vicious cycle of headache-medication-headache.
Identification from history:
Headache on ≥15 days/month for more than 3 months.
Regular overuse of acute/symptomatic headache medication for >3 months (e.g., simple analgesics on ≥15 days/month; triptans, opioids, combination analgesics on ≥10 days/month).
The headache develops or worsens during medication overuse.
The headache resolves or significantly improves within 2 months after discontinuing the overused medication.
Patients often describe a daily or near-daily headache, frequently present upon waking, which improves briefly with medication but then returns.
III. Examination & Investigations
Q1: What specific signs would you look for on neurological examination in a patient with headache? A1: I would conduct a focused neurological exam looking for:
Mental Status: Alertness, orientation, coherence (to rule out altered consciousness or delirium).
Cranial Nerves: Papilledema (optic nerve swelling - raised ICP), pupillary abnormalities (anisocoria, reactivity), extraocular movements (diplopia, nerve palsies), facial asymmetry, sensory deficits.
Motor System: Asymmetry in power, tone, reflexes (deep tendon reflexes, plantar reflex - focal neurological deficits).
Sensory System: Any sensory loss or asymmetry.
Cerebellar Signs: Ataxia, dysmetria, nystagmus (if cerebellar involvement suspected).
Meningeal Signs: Neck stiffness (nuchal rigidity), Kernig's sign, Brudzinski's sign.
Fundoscopy: Crucial for papilledema.
Temporal Artery Examination: Palpation for tenderness, thickening, or decreased pulse in GCA suspicion.
Q2: When would you consider neuroimaging (CT vs. MRI) for a patient presenting with headache? A2: Neuroimaging is indicated primarily for red flags or an atypical headache presentation.
Urgent CT scan (often non-contrast first): For acute severe headaches, especially thunderclap headache (to rule out SAH, intraparenchymal hemorrhage), new-onset headache with focal neurological deficits, altered mental status, or suspected acute stroke. It's faster and more readily available for emergencies.
MRI Brain (with/without contrast): Generally preferred for more subtle lesions, posterior fossa lesions, tumors, multiple sclerosis, chronic subdural hematomas, brain abscesses, or when CT is negative but clinical suspicion of serious pathology remains high (e.g., for vascular abnormalities like aneurysms, or inflammatory conditions). It offers better soft tissue resolution.
Q3: What are the indications for a lumbar puncture (LP) in a headache workup? What CSF findings would you expect in bacterial meningitis versus viral meningitis, or subarachnoid hemorrhage?
A3: Indications for LP in headache workup include:
Suspected meningitis/encephalitis (headache with fever, neck stiffness, altered mental status).
Suspected Subarachnoid Hemorrhage (SAH) where CT scan is negative but clinical suspicion remains high (LP performed 6-12 hours after onset to detect xanthochromia).
Suspected idiopathic intracranial hypertension (IIH).
Suspected low CSF pressure headache.
Some inflammatory/autoimmune neurological conditions.
CSF Findings:
Bacterial Meningitis: Turbid CSF, very high white blood cell count (WBC, predominantly neutrophils), very low glucose, very high protein, positive Gram stain/culture.
Viral Meningitis: Clear CSF, moderately elevated WBC (predominantly lymphocytes), normal glucose, mildly elevated protein, negative Gram stain/culture.
Subarachnoid Hemorrhage (SAH): Bloody CSF in all tubes (non-traumatic tap), and crucially, xanthochromia (yellowish discoloration due to bilirubin from lysed RBCs), which indicates that the blood has been in the CSF for some time (usually >6-12 hours).
Q4: A patient presents with headache, fever, and neck stiffness. What immediate investigations would you order, and what findings would confirm your suspicion?
A4: This triad strongly suggests meningitis.
Immediate Investigations:
Blood cultures: Before antibiotics.
STAT CT Brain: To rule out mass effect or contraindication to LP (e.g., hydrocephalus, large mass lesion).
Lumbar Puncture (LP): Once CT rules out contraindications, this is definitive.
Full Blood Count (FBC): Look for leukocytosis.
ESR/CRP: May be elevated.
Confirming Findings (from LP): The CSF analysis showing turbid appearance, markedly elevated WBC (predominantly neutrophils), low glucose, and high protein would strongly confirm bacterial meningitis. Gram stain or culture identifying a pathogen provides definitive diagnosis.
Q5: Discuss the role of ESR and CRP in headache workup.
A5: ESR (Erythrocyte Sedimentation Rate) and CRP (C-Reactive Protein) are non-specific inflammatory markers. Their primary role in headache workup is in the suspicion of Giant Cell Arteritis (GCA).
Elevated ESR (>50 mm/hr, often >100 mm/hr) and CRP in an older patient with new-onset headache (especially temporal or with jaw claudication/visual symptoms) is highly suggestive of GCA.
While not diagnostic on their own, significantly elevated values warrant immediate treatment with steroids and temporal artery biopsy to prevent irreversible vision loss. They can also be elevated in other systemic inflammatory or infectious causes of secondary headache, but GCA is the most critical to rule out rapidly in the context of new headache in the elderly.
IV. Pathophysiology & Specific Headache Disorders
Q1: Briefly explain the current understanding of migraine pathophysiology.
A1: Migraine pathophysiology is complex but largely involves the trigeminovascular system and central nervous system abnormalities. Key components include:
Cortical Spreading Depression (CSD): A wave of neuronal and glial depolarization that slowly spreads across the cerebral cortex, thought to underlie the migraine aura and possibly activate the trigeminal system.
Trigeminovascular System Activation: CSD, or other triggers, activates the trigeminal nerve, leading to release of neuropeptides like Calcitonin Gene-Related Peptide (CGRP) from perivascular nerve endings.
Neurogenic Inflammation: CGRP and other peptides cause vasodilation and inflammation in the meningeal blood vessels.
Sensitization: This peripheral activation leads to sensitization of second-order neurons in the trigeminal nucleus caudalis (TNC), contributing to pain perception. Further central sensitization can occur at higher brain centers, leading to allodynia (pain from non-painful stimuli) and photophobia/phonophobia.
Brainstem involvement: Hypothalamic and brainstem nuclei (e.g., dorsal raphe, locus coeruleus, periaqueductal gray) are implicated in initiating and modulating migraine attacks.
Q2: Describe the clinical features and pathophysiology of Cluster Headache. How does it differ from migraine?
A2:
Clinical Features: Cluster headache is characterized by severe, strictly unilateral pain (often orbital, supraorbital, or temporal) lasting 15-180 minutes, occurring in bouts (clusters) separated by remission periods. Attacks are typically accompanied by prominent ipsilateral autonomic symptoms (e.g., conjunctival injection, lacrimation, nasal congestion, rhinorrhea, facial sweating, ptosis, miosis, eyelid edema) and often restlessness or agitation. Attacks can occur multiple times a day.
Pathophysiology: Primarily involves the hypothalamus (suggested by its circadian rhythm and response to deep brain stimulation), leading to activation of the trigeminal autonomic reflex. The superior hypophyseal artery and cavernous sinus inflammation may also play a role.
Differences from Migraine:
Pain Quality: Excruciating, boring, non-pulsatile vs. throbbing.
Laterality: Strictly unilateral vs. often unilateral but can shift or be bilateral.
Associated Symptoms: Prominent ipsilateral autonomic features (tearing, congestion) vs. nausea/vomiting, photophobia/phonophobia.
Behavior: Restlessness/agitation vs. seeking quiet dark room.
Duration: Shorter (15-180 min) vs. longer (4-72 hrs).
Gender: More common in males vs. more common in females.
Circadian/Seasonal Rhythm: Distinct clusters vs. less predictable.
Q3: What is Trigeminal Neuralgia? How is it typically managed? A3: Trigeminal Neuralgia is a severe, debilitating condition characterized by sudden, usually unilateral, brief, excruciating, shock-like or stabbing pain in the distribution of one or more branches of the trigeminal nerve (V1, V2, or V3). It's typically triggered by innocuous stimuli like touching the face, chewing, talking, or brushing teeth. It's often caused by vascular compression of the trigeminal nerve root.
Management:
Medical: First-line is Carbamazepine or Oxcarbazepine. Other options include Gabapentin, Pregabalin, Baclofen, Lamotrigine.
Surgical (for refractory cases):
Microvascular Decompression (MVD): Most effective long-term treatment, separating the blood vessel from the nerve.
Gamma Knife Radiosurgery: Non-invasive, targets the nerve root.
Percutaneous procedures: Radiofrequency ablation, balloon compression, glycerol rhizolysis (less durable, higher recurrence).
Q4: Discuss headaches secondary to raised intracranial pressure (ICP). What are common causes, and how do these headaches typically present? A4: Headaches secondary to raised ICP are a significant concern.
Common Causes:
Mass lesions: Brain tumors (primary or metastatic), abscesses, hematomas.
Hydrocephalus: Obstructive or communicating.
Meningitis/Encephalitis: Causing brain edema or impaired CSF reabsorption.
Cerebral Venous Thrombosis (CVT): Obstructs venous outflow.
Idiopathic Intracranial Hypertension (IIH)/Pseudotumor Cerebri: Increased ICP without an obvious mass lesion.
Cerebral edema from various causes (e.g., trauma, stroke).
Typical Presentation:
Often dull, aching, diffuse headache.
Typically worse in the morning or when waking.
Aggravated by Valsalva maneuvers, coughing, sneezing, bending over.
May be associated with nausea and vomiting (especially projectile).
Crucially, associated with signs of raised ICP: papilledema (on fundoscopy), visual changes (blurred vision, diplopia), altered mental status.
Q5: Explain the concept of low CSF pressure headache. How does it present, and what are its common causes?
A5: Low CSF pressure headache (also known as spontaneous intracranial hypotension or headache due to CSF leak) occurs when there is a reduction in CSF volume or pressure, usually due to a leak.
Presentation: The hallmark is a postural headache, which is worse when upright (sitting or standing) and improves significantly when lying flat. It can range from dull to severe and may be associated with neck pain/stiffness, nausea, vomiting, dizziness, tinnitus, visual changes (e.g., diplopia), and hearing impairment.
Common Causes:
Spontaneous CSF leak: Often idiopathic, but can be due to ruptured meningeal diverticula, osteophytes, or trivial trauma.
Post-lumbar puncture headache: The most common iatrogenic cause.
Trauma or surgery involving the spine or head.
V. Management & Therapeutics
Q1: Outline the acute management strategy for a severe migraine attack. Include pharmacological and non-pharmacological options. A1: For severe migraine:
Non-pharmacological: Rest in a dark, quiet room; apply cold packs to the head; ensure adequate hydration.
Pharmacological:
First-line (severe attack): Triptans (e.g., Sumatriptan, Rizatriptan) – highly effective for aborting migraine pain and associated symptoms.
Combination analgesics: If triptans are contraindicated or ineffective (e.g., aspirin/acetaminophen/caffeine combination).
NSAIDs: (e.g., Ibuprofen, Naproxen) – effective for mild to moderate attacks or as adjunctive therapy.
Anti-emetics: (e.g., Metoclopramide, Prochlorperazine) – to manage nausea/vomiting and can also aid absorption of oral analgesics.
Corticosteroids (e.g., Dexamethasone): Can be used as rescue therapy to prevent recurrence in severe attacks.
CGRP receptor antagonists (gepants) or ditans: Newer oral acute treatments.
Q2: When would you initiate prophylactic therapy for migraine, and what are the first-line agents you would consider? A2: Prophylactic therapy for migraine is generally initiated when:
Migraine attacks are frequent (e.g., ≥4 attacks per month).
Attacks are long-lasting (e.g., >12 hours), severe, or cause significant disability.
Acute treatments are ineffective, contraindicated, or overused.
The patient expresses a strong preference for prevention.
First-line prophylactic agents:
Beta-blockers: Propranolol, Metoprolol.
Anticonvulsants: Topiramate, Valproate (caution in women of childbearing age due to teratogenicity).
Tricyclic Antidepressants (TCAs): Amitriptyline (especially if co-existing depression/insomnia).
CGRP monoclonal antibodies: (e.g., Erenumab, Fremanezumab, Galcanezumab) – newer, highly effective injectables.
Q3: How would you manage a patient with chronic tension-type headache (CTTH)?
A3: Managing CTTH typically involves a multi-modal approach:
Education & Lifestyle: Stress management, regular sleep, regular meals, hydration, regular exercise.
Non-pharmacological: Physical therapy, biofeedback, cognitive-behavioral therapy (CBT), acupuncture, relaxation techniques.
Pharmacological (Prophylaxis):
First-line: Amitriptyline (low dose).
Other options: Mirtazapine, Venlafaxine, or other TCAs/SNRIs.
Acute Treatment: Judicious use of simple analgesics (paracetamol, NSAIDs) but strictly limit frequency to avoid Medication Overuse Headache. Avoid opioids.
Q4: Describe the acute and prophylactic management of Cluster Headache.
A4:
Acute Management:
High-flow Oxygen (100% at 12-15 L/min for 15-20 min): Often very effective, first-line non-pharmacological.
Subcutaneous Sumatriptan: Rapid onset, highly effective.
Intranasal triptans (e.g., Zolmitriptan) or oral triptans (less rapid onset).
Prophylactic Management (for a cluster period):
First-line: Verapamil (calcium channel blocker) – often started with ECG monitoring.
Steroids (e.g., Prednisolone taper): Used as a bridge while waiting for Verapamil to take effect.
Other options: Lithium, Topiramate.
Long-term refractory cases: Greater occipital nerve block, deep brain stimulation (rare).
Q5: Discuss the management of a patient presenting with Thunderclap Headache, assuming investigations confirm a benign cause versus a serious one.
A5:
Initial Approach (Always assume serious until proven otherwise):
Immediate non-contrast CT Brain: To rule out SAH, intraparenchymal hemorrhage.
If CT is negative but suspicion remains (e.g., within 6-12 hours of onset), perform a Lumbar Puncture (LP) to check for xanthochromia.
Consider CT Angiography (CTA) or MR Angiography (MRA) of brain vessels to rule out aneurysms, dissections, or RCVS.
Treat symptoms (pain, nausea) while investigations are ongoing.
Management if Serious Cause Confirmed (e.g., SAH):
Neurosurgical consultation for aneurysm clipping or coiling.
Intensive care monitoring for vasospasm, hydrocephalus, re-bleeding.
Strict blood pressure control.
Management if Benign Cause Confirmed (e.g., Primary Thunderclap Headache, Benign Cough/Exertional Headache):
Reassurance: Crucially, reassure the patient that a life-threatening cause has been excluded.
Symptomatic relief: NSAIDs, triptans if features of migraine are present.
Prophylaxis (if recurrent): Indomethacin is often effective for primary cough or exertional headaches. Beta-blockers or calcium channel blockers can be considered.
Patient education: Advise on avoidance of specific triggers if identified.
VI. Advanced & Challenging Scenarios
Q1: Discuss headache in pregnancy. What are the unique considerations and management challenges? A1: Headache is common in pregnancy. Unique considerations and challenges include:
Physiological changes: Hormonal fluctuations, fluid retention, blood volume changes.
Red flags are critical: New-onset or severe headaches, especially in the third trimester or postpartum, can indicate serious conditions like pre-eclampsia/eclampsia, cerebral venous thrombosis, reversible cerebral vasoconstriction syndrome, pituitary apoplexy, or SAH. Thorough investigation is mandatory.
Medication restrictions: Many standard headache medications are contraindicated or have limited safety data in pregnancy.
Acute: Acetaminophen is generally safe. NSAIDs are avoided in the third trimester. Triptans are used with caution (Sumatriptan has the most data). Opioids are generally avoided.
Prophylactic: Beta-blockers (e.g., Propranolol) are relatively safe. Amitriptyline can be considered. Topiramate and Valproate are generally contraindicated due to teratogenicity. CGRP monoclonal antibodies have limited pregnancy data.
LP and imaging: MRI is generally safe in pregnancy (avoiding gadolinium in 1st trimester if possible). CT is used if benefits outweigh risks, with abdominal shielding. LP is safe if indicated.
Q2: How would you approach a patient presenting with daily headache that doesn't fit typical primary headache criteria?
A2: A daily headache that doesn't fit typical patterns is concerning for chronic daily headache (CDH) or a secondary cause.
Rule out secondary causes (RED FLAGS): This is paramount. Look diligently for any SNOOP10 red flags that might suggest a tumor, hydrocephalus, IIH, chronic subdural, etc. Perform neurological exam and consider neuroimaging.
Evaluate for Medication Overuse Headache (MOH): This is a very common cause of CDH. Detailed medication history is essential.
Thorough Headache Phenotyping: Even if atypical, try to classify it as chronic migraine, chronic tension-type, or New Daily Persistent Headache (NDPH).
Psychological Assessment: Assess for anxiety, depression, and stress, which often co-exist and contribute to CDH.
Management:
If MOH: Withdrawal of overused medication is critical, often the most challenging step. Provide a "detox" plan.
If NDPH or chronic migraine/TTH: Initiate appropriate prophylactic therapy (e.g., amitriptyline, topiramate, CGRP mAbs for chronic migraine).
Multidisciplinary approach: Consider referral to a pain clinic, neurologists specializing in headache, psychologists/psychiatrists for CBT or stress management.
Focus on non-pharmacological strategies and lifestyle modification.
Q3: What are the specific headache types associated with Systemic Lupus Erythematosus (SLE) or other systemic inflammatory conditions? How do you manage them?
A3: Headaches in SLE or other systemic inflammatory conditions (e.g., rheumatoid arthritis, vasculitis) can be:
Primary headaches: Migraine or tension-type, often exacerbated by the underlying inflammatory state.
Secondary headaches directly related to the systemic disease:
CNS vasculitis: Causing ischemia or hemorrhage.
Infections: Due to immunosuppression.
Increased ICP: From hydrocephalus, cerebral edema, or aseptic meningitis.
Cerebral venous thrombosis.
Drug-induced headaches: From medications used to treat the systemic condition (e.g., corticosteroids withdrawal, methotrexate).
Management:
Rule out serious secondary causes: Always investigate vigorously with imaging and LP if suspicion is high.
Treat the underlying systemic disease: Optimizing control of SLE or other inflammatory conditions with disease-modifying agents (e.g., corticosteroids, immunosuppressants) is crucial.
Symptomatic management: For primary-like headaches, use standard migraine/TTH treatments, being mindful of drug interactions and side effects given the patient's other medications.
Consider specific treatments if due to vasculitis (e.g., higher dose steroids, cyclophosphamide).
Q4: Describe the approach to a patient presenting with headache and visual symptoms.
A4: Headache with visual symptoms warrants careful evaluation as it can range from benign migraine aura to sight-threatening conditions.
Detailed History:
Nature of visual symptoms: Flashing lights, zigzag lines (aura), blurred vision, diplopia, transient monocular blindness (amaurosis fugax), visual field loss.
Onset and timing: Before, during, or after headache? Gradual or sudden? Transient or persistent?
Associated with specific triggers/aggravating factors.
Age and comorbidities: (e.g., >50 years - GCA, hypertension/diabetes - TIA/stroke risk).
Thorough Examination:
Full neurological exam: Especially cranial nerves (II, III, IV, VI).
Fundoscopy: Absolutely critical for papilledema (raised ICP) or retinal abnormalities (e.g., emboli in amaurosis fugax).
Visual acuity and visual fields testing.
Temporal artery palpation (for GCA).
Differential Diagnosis:
Migraine with Aura: Most common benign cause.
Giant Cell Arteritis (GCA): Urgent, potentially blinding.
Acute Angle-Closure Glaucoma: Painful red eye, halos.
Stroke/TIA: Especially posterior circulation events.
Mass lesions/Raised ICP: Causing papilledema or cranial nerve palsies.
Optic neuritis/Multiple Sclerosis.
Reversible Cerebral Vasoconstriction Syndrome (RCVS).
Investigations: Based on suspicion, consider urgent neuroimaging (CT/MRI), CTA/MRA, ESR/CRP, ophthalmological consultation.
Q5: A patient on long-term anticoagulation presents with a new-onset headache. What is your immediate concern and plan of action?
A5:
Immediate Concern: The primary immediate concern is intracranial hemorrhage (ICH), including subdural hematoma, epidural hematoma, or intraparenchymal hemorrhage, due to the anticoagulation. Even minor head trauma can lead to significant bleeding in these patients. Cerebral venous thrombosis is also a possibility.
Plan of Action:
STAT Non-contrast CT Brain: This is the most crucial initial investigation to quickly rule out acute hemorrhage.
Check Coagulation Status: Immediately send blood for INR (if on Warfarin), aPTT (if on Heparin), or specific assays for Direct Oral Anticoagulants (DOACs) if available.
Reverse Anticoagulation (if active bleed suspected/confirmed):
For Warfarin: Vitamin K, Prothrombin Complex Concentrate (PCC).
For Heparin: Protamine Sulfate.
For DOACs: Specific reversal agents if available (e.g., Idarucizumab for Dabigatran, Andexanet alfa for Factor Xa inhibitors) or PCC.
Neurological Consultation: Involve neurology/neurosurgery immediately.
Supportive Care: Manage blood pressure, maintain airway, breathing, circulation.
Close Monitoring: Serial neurological exams.