Neurology: Essential Evaluation Frameworks
Evaluation of Headache
History and Presenting Features
A systematic headache history requires understanding the temporal pattern and character of pain. Begin by establishing onset timing—whether symptoms developed suddenly over seconds to minutes or gradually over hours to days. This temporal relationship often guides your diagnostic thinking. Characterize the pain quality using patient language: pressure, throbbing, stabbing, or burning sensations provide clues. Determine location with precision, noting whether pain is unilateral or bilateral, frontal, temporal, occipital, or generalized.
Establish severity using a numeric scale (0-10), duration of individual episodes and total illness duration, and identifiable triggers such as stress, sleep deprivation, menses, or positional changes. Explore associated symptoms systematically: floaters or visual changes, nausea and vomiting, photophobia and phonophobia, and any focal neurologic deficits.
Red Flag Symptoms Requiring Urgent Evaluation
Headache Red Flags
- Focal neurologic deficit or weakness
- Altered mental status or confusion
- Seizure activity
- Vision changes or diplopia
- Meningeal signs (neck stiffness)
- Fever
- Positional relationship to symptoms
- Progressive worsening
- Papilledema on fundoscopy
- Thunderclap onset (sudden maximal intensity)
Primary Headache Disorders
| Headache Type | Characteristics | Typical Triggers | Treatment |
|---|---|---|---|
| Tension | Bilateral pressure or band-like sensation; mild to moderate severity; no prodrome | Stress, sleep deprivation, muscle tension | NSAIDs, acetaminophen; tricyclic antidepressants (amitriptyline) for chronic |
| Cluster | Unilateral periorbital/temporal pain; autonomic features (rhinorrhea, conjunctival injection, lacrimation, miosis, ptosis) | Alcohol, nitrates | High-flow oxygen (15L/min); subcutaneous sumatriptan; prednisone 60mg once daily for acute cluster |
| Migraine | Unilateral throbbing pain; often preceded by aura (visual, sensory, speech); 4-72 hour duration; nausea/vomiting | Hormonal changes, sleep disruption, weather changes | Triptans (5HT1 agonists); acetaminophen + caffeine combinations; IV options (DHE, ketorolac) for severe episodes |
Secondary Headache Causes
| Category | Conditions | Key Distinguishing Features |
|---|---|---|
| Traumatic | Post-concussive headache, subarachnoid hemorrhage, subdural hematoma | Recent head trauma; thunderclap onset for SAH |
| Increased ICP | Brain tumor, hydrocephalus, pseudotumor cerebri | Progressive symptoms, morning symptoms, papilledema |
| Decreased ICP | Post-lumbar puncture, CSF leak | Recent LP or dural puncture; positional quality |
| Vascular | Acute stroke, arterial dissection, vasculitis, temporal arteritis | Age >50, focal deficits, vision loss, jaw claudication |
| Meningeal | Bacterial meningitis, viral meningitis, subarachnoid hemorrhage | Fever, neck stiffness, photophobia |
| Extracranial | Sinusitis, temporomandibular joint dysfunction, glaucoma | Facial pressure, jaw pain, eye pain with vision changes |
| Systemic | Hypoxia, uncontrolled hypertension, hypoglycemia | Associated systemic symptoms |
| Medication-Related | Medication overuse headache, withdrawal syndromes | Frequent analgesic use; recent medication changes |
Diagnostic Approach
Headache Workup Strategy
- Imaging First: Non-contrast CT brain for acute presentation with concerning features (thunderclap, focal deficits, altered mental status)
- MRI Brain: When structural lesion suspected but CT normal; migraines with atypical features
- Lumbar Puncture: If febrile with meningeal signs or suspected SAH with negative CT imaging
- Labs: ESR and CRP for temporal arteritis suspicion (especially age >50)
- Specialty Imaging: CTA/MRA for vascular concerns; CT sinuses for sinusitis
Evaluation of Syncope
Syncope results from transient cerebral hypoperfusion. Understanding the mechanism guides management and risk stratification. The WOMAN PE framework organizes the major etiologic categories.
Syncope Etiology Framework: WOMAN PE
| Category | Mechanism | Clinical Features |
|---|---|---|
| W - Neurally Mediated | Vagal/neural reflex activation | Prodromal symptoms (palpitations, nausea, diaphoresis); recurrent episodes; situational or positional triggers |
| O - Orthostatic | Inability to maintain blood pressure on position change | Symptoms with standing; improvement with lying down; often elderly or dehydrated |
| M - Mechanical (FATAL) | Structural obstruction to cardiac output | Exertional onset; cardiac murmur; no prodrome; family history of sudden death |
| A - Arrhythmia (FATAL) | Abnormal heart rhythm | Sudden onset without prodrome; palpitations; syncope during sleep possible |
| V - Vascular | Acute vascular compromise | Focal neurologic deficits; chest pain; risk factors for dissection |
| P - Psychiatric | Psychogenic non-epileptic seizure (pseudoseizure) | Gradual onset; variable presentation; often younger patients |
| E - Endocrine/Other | Metabolic or medication-related | Hypoglycemia, electrolyte abnormalities, medication effects |
Evaluation by Etiology
| Etiology | Initial Testing | Additional Workup |
|---|---|---|
| Neurally Mediated | Orthostatic vital signs; history of prodrome | Tilt table test if diagnosis uncertain; conservative management |
| Orthostatic | Supine/standing blood pressure (≥20 mmHg systolic or ≥10 mmHg diastolic drop); assess volume status | IV fluid repletion; compression stockings; medication review |
| Mechanical (Exertional, Murmur) | ECG; cardiac auscultation | Transthoracic echocardiography; cardiology consultation |
| Arrhythmia | 12-lead ECG; continuous telemetry | Holter monitor; event monitor; electrophysiology consultation |
| Vascular (Focal Deficits) | Careful neurologic examination | CTA neck/chest; carotid ultrasound; neurology consultation |
Comprehensive Syncope Workup
Syncope Investigation Protocol
- Labs: CBC, comprehensive metabolic panel, glucose level, pregnancy test (if applicable)
- Cardiac: 12-lead ECG, continuous telemetry monitoring, troponin
- Imaging: Chest X-ray; consider D-dimer if VTE suspected; consider troponin elevation
- Specialized: EEG if seizure suspected; carotid ultrasonography; brain imaging if focal deficits
- Risk Stratification: Presence of cardiac etiology indicates higher risk of adverse outcomes
Altered Mental Status and Delirium
Delirium represents acute dysfunction of consciousness and cognition. Understanding the spectrum of mental status changes and systematic etiologic search are essential.
Spectrum of Altered Mental Status
Progress from hyperalert (agitation, hallucinations) through confusion and true delirium, then to progressive somnolence: lethargic (falls asleep easily but awakens to stimulation), obtunded (awakens only to vigorous stimulation), stuporous (minimal response to painful stimuli only), and finally comatose (no purposeful response to external stimuli).
Etiologic Framework: "HE STOPS for TIPS on AEIOUS"
- H: Hepatic encephalopathy, Hypertensive emergency
- E: Electrolyte abnormalities
- S: Stroke, Subdural hematoma, Subarachnoid hemorrhage
- T: Trauma, Temperature extremes
- O: Opioid toxicity, Overdose of other medications
- P: Psychiatric illness
- S: Seizure activity, Sepsis, Syphilis (neurosyphilis)
- T: Thyroid dysfunction (hyper and hypothyroid), Toxic ingestion
- I: Infection (UTI, pneumonia, meningitis), Intracranial process, Increased ICP
- P: Porphyria
- S: Systemic acidosis
- A: Anemia, Anoxia, Acidosis
- E: Endocrine disorders (hypoglycemia, DKA, HHS)
- I: Intoxication (alcohol, drugs), Intracranial hemorrhage
- O: Opioid toxicity, Oxygen hypoxia, Osmolality (hyponatremia)
- U: Uremia
- S: Seizure, Stroke, Subdural
Glasgow Coma Scale
The GCS quantifies level of consciousness using eye opening, verbal response, and motor response.
| Component | Scoring (out of 15 total) |
|---|---|
| Eye Opening (E: 1-4) | 4 = Spontaneous; 3 = To verbal command; 2 = To pain; 1 = No response |
| Verbal Response (V: 1-5) | 5 = Oriented; 4 = Confused; 3 = Inappropriate words; 2 = Incomprehensible; 1 = No response |
| Motor Response (M: 1-6) | 6 = Obeys commands; 5 = Localizes to pain; 4 = Withdraws from pain; 3 = Abnormal flexion; 2 = Abnormal extension; 1 = No response |
Interpretation: 15 = Normal function; 13-14 = Minor impairment; 9-12 = Moderate impairment; ≤8 = Severe impairment/comatose state
Neurologic Examination in Altered Mental Status
| Exam Component | Findings and Interpretation |
|---|---|
| Mental Status | Document GCS score; assess orientation to person, place, time; evaluate attention and memory |
| Pupils | Pinpoint = opioid intoxication or pontine hemorrhage; mid-fixed = midbrain injury; dilated and fixed = anoxic injury, herniation, or anticholinergic toxicity |
| Extraocular Movements | Doll's eyes (oculocephalic reflex) and cold calorics (oculovestibular reflex) assess brainstem function; absence suggests brainstem injury |
| Motor/Sensory | Assess for focal deficits suggesting stroke; check for meningeal signs (neck stiffness, Kernig, Brudzinski) |
| Reflexes | Brisk reflexes may suggest metabolic derangement; diminished reflexes suggest toxic ingestion |
Diagnostic Workup
AMS Investigation Sequence
- Universal Labs: CBC, comprehensive metabolic panel, urinalysis (all patients)
- Toxins: Urine drug screen, blood alcohol level
- Targeted Labs (based on history/exam):
- Hepatic encephalopathy: serum ammonia, liver function tests
- Endocrine: TSH, serum/urine osmolality, cortisol
- Nutritional: B12 level, folate
- Acidosis: arterial blood gas
- Imaging: Non-contrast CT head for acute presentation; MRI if CT normal but high suspicion for structural disease
- Lumbar Puncture: If meningitis/encephalitis suspected after imaging excludes mass
- EEG: For suspected seizure activity; encephalitis; myxedema coma
Management Principles
Acute AMS Management
- Discontinue any medication that could precipitate altered mental status
- Administer thiamine 100 mg IV (prevents Wernicke encephalopathy)
- Administer dextrose (D50) if hypoglycemia present (after thiamine to prevent Wernicke)
- Consider naloxone if opioid intoxication suspected
- Maintain cervical spine immobilization if trauma concern
- Elevate head of bed and manage increased ICP if indicated
Evaluation of Stroke
Stroke represents acute neurologic deficit from vascular origin. Rapid identification of stroke type and vascular territory guides acute intervention.
Stroke Classification
- TIA (Transient Ischemic Attack): Transient neurologic symptoms with negative imaging; resolution within 24 hours
- Ischemic Stroke (85% of cases):
- Embolic: Cardioembolic source (atrial fibrillation, valvular disease); arterial embolus
- Thrombotic: Atherosclerotic disease; lacunar infarction
- Hemorrhagic Stroke (15% of cases):
- Intracerebral hemorrhage (hypertension, amyloid angiopathy)
- Subarachnoid hemorrhage (ruptured aneurysm, AVM)
Vascular Territory and Clinical Syndromes
| Vessel | Territory | Clinical Presentation |
|---|---|---|
| ICA/Ophthalmic | Retina | Amaurosis fugax (transient monocular vision loss) |
| ACA (Anterior Cerebral Artery) | Medial frontal/parietal | Leg hemiplegia > arm; urinary incontinence; personality change |
| MCA (Middle Cerebral Artery) | Lateral cortex/basal ganglia | Face/arm hemiplegia > leg; aphasia (dominant hemisphere) or neglect (nondominant) |
| PCA (Posterior Cerebral Artery) | Occipital lobe | Homonymous hemianopia with macular sparing; visual hallucinations |
| Vertebral/PICA (Wallenberg) | Lateral medulla | Ipsilateral facial numbness; contralateral body numbness; Horner syndrome; intractable hiccups |
| Basilar Artery | Brainstem (pons, midbrain) | Locked-in syndrome (at midbrain level); quadriplegia; CN abnormalities; altered consciousness |
| Cerebellar | Cerebellum | Vertigo, nausea/vomiting; diplopia; ipsilateral ataxia; headache |
| Lacunar | Small penetrating vessels | 5 classic syndromes: pure motor; pure sensory; ataxic hemiparesis; dysarthria-clumsy hand; mixed sensorimotor |
NIH Stroke Scale (NIHSS)
The NIHSS quantifies stroke severity across 11 items (1a through 11). Reference the NIH Stroke Scale on MDCalc for detailed scoring. Higher scores correlate with larger infarct volume and worse outcomes.
Acute Stroke Diagnostic Workup
Stroke Evaluation Protocol
- Labs: CBC, comprehensive metabolic panel, coagulation studies (PT/PTT), ECG, troponin, toxicology screen
- Monitoring: Continuous cardiac telemetry
- Imaging: Stat non-contrast CT head (rule out hemorrhage); CTA head/neck if large vessel occlusion symptoms present
- ICU Criteria: tPA recipients; worsening strokes; hemorrhagic strokes; requiring vasopressor support
tPA Eligibility Criteria
Alteplase (tPA) represents standard care for eligible acute ischemic stroke.
tPA Contraindications and Timing
- Timing: Within 4.5 hours from symptom onset
- Blood Pressure: Must be <185/110 mmHg (uncontrolled hypertension is absolute contraindication)
- Platelet Count: ≥100,000 (severe thrombocytopenia contraindication)
- Coagulation: INR ≤1.7 if on warfarin
- Bleeding Risk: No recent surgery, intracranial hemorrhage, GI bleeding, or active bleeding
- Other: No seizure at stroke onset; blood glucose >50 and <400 mg/dL
Last update:
April 12, 2026