Neurology

• Sudden unilateral weakness or numbness (arm, leg, face)
• Facial droop - forehead movement preserved (upper motor neuron pattern)
• Slurred speech (dysarthria) or inability to find words (aphasia)
• Gaze deviation toward the side of the lesion
• Sudden vision changes (monocular or hemianopia)
• Sudden severe headache (less common - more typical of hemorrhagic)

vs. Bell's palsy: In ischemic stroke, the forehead is SPARED (patient can still wrinkle their forehead). In Bell's palsy, the entire face is involved - patient cannot raise their eyebrow. This single finding separates a peripheral cranial nerve VII lesion from a central stroke.

Time is brain. Every minute without reperfusion destroys roughly 1.9 million neurons. Last-known-well time is the critical data point - document it precisely. Thrombolytic window: within 3 hours of onset (extended to 4.5 hours for selected patients). Endovascular thrombectomy may be an option up to 24 hours in selected large-vessel occlusions. Many systems now use tenecteplase (TNK) in place of alteplase.

• "Worst headache of life" - sudden, maximal-intensity (subarachnoid)
• Rapid onset of focal neurological deficits
• Nausea and vomiting (elevated ICP)
• Altered mental status; may deteriorate quickly
• Cushing's Triad (hypertension + bradycardia + irregular respirations) - late sign of herniation
• Neck stiffness (subarachnoid - meningeal irritation)

vs. Ischemic stroke: Hemorrhagic strokes typically have a more sudden, severe onset - often the headache is described before any deficit. Cushing's Triad indicates herniation and is absent in ischemic stroke. CT is required to differentiate; field management is similar - maintain airway, avoid hypotension.

Cushing's Triad = impending transtentorial herniation. These patients require immediate airway management. Avoid hypotension - permissive hypertension is appropriate in the field unless extreme. Do NOT give thrombolytics (contraindicated).

• Focal neurological deficit identical to ischemic stroke in presentation
• Symptoms resolve completely - typically within minutes to hours
• No infarct on imaging (by definition - diagnosed retrospectively)
• Patient may present after symptoms have resolved ("I felt fine, thought it was nothing")
• Age, hypertension, atrial fibrillation, and carotid disease are common risk factors
• May have amaurosis fugax (transient monocular blindness)

vs. Completed stroke: TIA is defined retrospectively when deficits fully resolve within 24 hours. In the field, the presentation is indistinguishable from stroke. Treat all TIAs as stroke in progress - transport urgently. Do not reassure the patient that because symptoms resolved, the event is insignificant.

TIA carries a 10-15% stroke risk within the following 90 days, with peak risk in the first 48 hours. Patients who "feel fine now" require the same urgency as active stroke. Transport and evaluate - do not leave on scene.

• Generalized tonic-clonic: LOC, rigid stiffening → rhythmic limb jerking, tongue biting, incontinence
• Post-ictal phase: confusion, fatigue, deep sleep - may last minutes to hours
• Focal (partial): involuntary movement or sensory changes in one body region; awareness may be preserved or impaired
• Absence: brief staring spell, no postictal phase, more common in children
• Status epilepticus: continuous seizure activity >5 minutes, or two seizures without return to baseline
• Todd's paralysis: transient unilateral weakness after a focal seizure

vs. Syncope: Seizure has a postictal phase, tongue biting, incontinence, and muscle soreness. Syncope recovers almost immediately without confusion. Todd's paralysis (post-seizure focal weakness) mimics stroke - check glucose first.

Status epilepticus >30 minutes causes irreversible brain injury. Benzodiazepines (diazepam, midazolam, lorazepam) are first-line field treatment. Do not wait - administer early in all prolonged seizures.

• Confusion, disorientation (person, place, time, event)
• Agitation, combativeness, or paradoxical calm
• Decreased responsiveness on AVPU scale
• Speech changes: slurring, incoherence, reduced output
• Use AEIOU-TIPS: Alcohol, Epilepsy, Insulin, Opiates, Uremia, Trauma, Infection, Psychiatric, Stroke/Structural
• New AMS in elderly without obvious cause = sepsis until proven otherwise

vs. Primary psychiatric cause: Always rule out metabolic, toxic, and structural causes before attributing AMS to psychiatry. Check glucose, SpO2, temperature, and pupils on every patient with AMS. Organic cause missed = potential patient death.

New AMS in an elderly patient without an obvious explanation is sepsis until proven otherwise. Elderly patients rarely present with the classic fever + source pattern - AMS may be their only sign of severe systemic infection.

• Unilateral facial weakness involving BOTH upper and lower face (including forehead)
• Inability to close the eye completely (lagophthalmos)
• Drooping of the corner of the mouth
• Loss of the nasolabial fold on affected side
• May have ipsilateral ear pain (viral reactivation - herpes zoster)
• Onset over hours to days (less sudden than stroke)

vs. Ischemic stroke: This is the highest-yield neuro differential on the NREMT. In Bell's palsy, the forehead is INVOLVED - the patient cannot raise the eyebrow. In central stroke, the forehead is SPARED - the patient can still wrinkle it. One finding, clear answer.

If the forehead is SPARED - assume central stroke and treat accordingly. Never diagnose Bell's palsy in the field without confirming the forehead is equally affected. When in doubt, it is a stroke until the ED says otherwise.