14.2 Neurological Emergencies: Stroke Syndromes, TIA, Seizures & Status Epilepticus

14.2 Neurological Emergencies: Stroke Syndromes, TIA, Seizures & Status Epilepticus

Pathophysiology of Acute Cerebrovascular Syndromes

Acute cerebrovascular accidents (strokes) represent the third leading cause of death and the primary cause of acquired long-term adult disability in Canada. Rapid prehospital identification, accurate anatomical localization, and coordinated system-level routing under Canadian Stroke Best Practice Recommendations (CPCF Appendix A #4, #7) dictate patient neurological survival.

Strokes are broadly categorized into two distinct pathophysiological mechanisms:

1. Ischemic Stroke (~85% of cases): Arises from sudden occlusion of a cerebral artery by a thrombus (formed locally over a ruptured atherosclerotic plaque) or an embolus (originating from atrial fibrillation, left ventricular mural thrombi, or carotid atheroma). Occlusion precipitates a central ischemic core—tissue where cerebral blood flow drops below 10–12 mL/100g/min, causing rapid cellular ATP exhaustion, cytotoxic edema, membrane depolarization, and irreversible neuronal necrosis within minutes. Surrounding this necrotic core lies the ischemic penumbra—hypoperfused, electrically silent brain tissue that remains biochemically viable via leptomeningeal collateral vessels. Prehospital care is entirely dedicated to rescuing the ischemic penumbra through rapid reperfusion and physiological support.
2. Hemorrhagic Stroke (~15% of cases): Involves mechanical disruption of a cerebral vessel with extravasation of blood directly into brain parenchyma (Intracerebral Hemorrhage [ICH]) or into the subarachnoid space (Subarachnoid Hemorrhage [SAH]). ICH typically results from chronic hypertensive arteriopathy rupturing Charcot-Bouchard microaneurysms in penetrating basal ganglia arteries. SAH classically arises from the rupture of a saccular (berry) aneurysm on the circle of Willis, presenting with an instantaneous 'thunderclap' headache, meningismus, and rapid loss of consciousness. Hemorrhage causes both direct mechanical tissue destruction and precipitous elevations in Intracranial Pressure (ICP), compressing adjacent microvasculature and causing secondary brain herniation.

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Prehospital Stroke Assessment & Large Vessel Occlusion (LVO) Screening

Time is brain: during an acute ischemic stroke, an estimated 1.9 million neurons, 14 billion synapses, and 12 km of myelinated fibers are lost every minute. Paramedics must execute rapid, standardized clinical screening.

1. Prehospital Stroke Screening Tools (FAST & CPSS)

The FAST protocol (Face, Arm, Speech, Time) and the Cincinnati Prehospital Stroke Scale (CPSS) evaluate three cardinal neurological signs:

• Facial Droop: Asymmetrical smile or grimace (cranial nerve VII motor deficit).
• Arm Drift: Inability to hold both arms extended palms-up for 10 seconds without downward drift or pronation.
• Abnormal Speech: Dysarthria (slurred speech) or expressive/receptive dysphasia when repeating a standard sentence ('You can't teach an old dog new tricks').

The presence of any one of these three abnormal findings possesses an 88% sensitivity for acute stroke.

2. Establishing the Exact Last Seen Normal (LSN) Window

The Last Seen Normal (LSN) time is defined as the exact time the patient was last witnessed by reliable collateral observers to be at their neurological baseline, free of any focal deficits:

• If a patient awakens with stroke symptoms ('Wake-Up Stroke'), the LSN is recorded as the time the patient went to bed or was last seen awake and normal, NOT the time of awakening.
• Intravenous Thrombolytic Window: Systemic thrombolysis with tenecteplase (TNK) or alteplase (tPA) is authorized within 4.5 hours of LSN.
• Endovascular Thrombectomy (EVT) Window: Mechanical clot retrieval with stent-retrievers is indicated up to 6 hours, and in select patients with salvageable penumbra on perfusion neuroimaging, up to 24 hours from LSN.

3. Large Vessel Occlusion (LVO) Assessment Tools

Proximal occlusions of the internal carotid artery (ICA) or the M1/M2 segments of the middle cerebral artery (MCA) carry devastating mortality (~80% poor outcome if untreated with IV thrombolysis alone). Prehospital scales detect 'cortical signs' indicative of LVO:

Los Angeles Motor Scale (LAMS) Scoring:
- Facial Droop: Absent (0), Present (1)
- Arm Drift: Absent (0), Drifts down before 10 sec (1), Falls rapidly or no effort (2)
- Grip Strength: Normal (0), Weak grip (1), No grip / flaccid (2)
Interpretation: Total score ranges from 0 to 5. A LAMS score >= 4 indicates high probability of LVO.

Alternative validated Canadian scales include ACT-FAST (Automated Clinical Triage for Acute Stroke Therapy) and VAN (Vision, Aphasia, Neglect). When LVO screening is positive and LSN is within the eligible window (typically <6–24 hours), prehospital stroke bypass protocols mandate routing the patient directly to a Comprehensive Stroke Centre with 24/7 EVT capabilities, bypassing primary stroke facilities.

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Blood Pressure Management in Acute Ischemic Stroke: Permissive Hypertension

A pivotal principle of neuroresuscitation is maintaining Cerebral Perfusion Pressure (CPP):

$\text{CPP} = \text{Mean Arterial Pressure (MAP)} - \text{Intracranial Pressure (ICP)}$

In the healthy brain, autoregulation maintains constant cerebral blood flow across MAPs ranging from 60 to 150 mmHg. In acute ischemic stroke, autoregulation is completely abolished within the ischemic penumbra; capillary perfusion becomes entirely passive and directly dependent on systemic blood pressure driving collateral flow.

Elevated systemic blood pressure is a protective physiological reflex to maintain collateral flow across the circle of Willis. Excessive or rapid blood pressure reduction causes immediate hypoperfusion, transforming viable penumbra into irreversible necrotic infarction.

[!CAUTION] Avoid Prehospital Antihypertensives: Canadian prehospital guidelines dictate that paramedics must NEVER administer antihypertensive medications to lower blood pressure in acute ischemic stroke unless specific medical direction is provided. Standard guidelines permit permissive hypertension up to SBP 220 mmHg and DBP 120 mmHg in non-thrombolysis candidates (or SBP <185 mmHg and DBP <110 mmHg if preparing for IV thrombolysis under direct in-hospital stroke team protocol).

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Transient Ischemic Attack (TIA): Recognition & Risk Stratification

A Transient Ischemic Attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute tissue infarction on magnetic resonance imaging (MRI). While symptoms traditionally resolve completely within minutes to hours (typically <1 hour), a TIA represents an unstable vascular emergency.

• Stroke Recurrence Risk: Up to 10% to 15% of TIA patients suffer a full, disabling ischemic stroke within 90 days, with the highest clustering of risk occurring in the first 48 hours.
• The ABCD2 Risk Stratification Score: Paramedics and receiving emergency physicians assess risk using the ABCD2 score:
  • Age: >= 60 years (1 point)
  • Blood Pressure: SBP >= 140 or DBP >= 90 mmHg (1 point)
  • Clinical Features: Unilateral motor weakness (2 points) or isolated speech disturbance without weakness (1 point)
  • Duration of symptoms: >= 60 minutes (2 points) or 10–59 minutes (1 point)
  • Diabetes mellitus: History of diabetes (1 point)
• An ABCD2 score >= 4 designates high short-term stroke risk, necessitating emergent neurological workup, urgent vascular imaging (carotid Doppler/CT angiography), and initiation of dual antiplatelet therapy.

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Seizures: Pathophysiology, Clinical Phases & Status Epilepticus

A seizure is a transient occurrence of signs and symptoms resulting from abnormal, excessive, and hypersynchronous electrical discharges of cortical neurons. Epilepsy is a chronic disorder characterized by recurrent unprovoked seizures, but acute seizures frequently stem from acute systemic or intracranial insults.

Phases of a Generalized Tonic-Clonic Seizure (GTCS)

1. Aura: Focal onset reflecting the localized anatomical origin of the epileptic focus (e.g., epigastric rising sensation, olfactory hallucinations, psychic déjà vu). Not all seizures exhibit an aura.
2. Tonic Phase (10 to 30 seconds): Generalized, sustained contraction of the entire musculature. Increased intrathoracic pressure forces air across closed vocal cords, producing the classic 'epileptic cry'. The patient becomes rigid, exhibits decerebrate posturing, experiences respiratory arrest with cyanosis, and bites the tongue (classically lateral tongue border).
3. Clonic Phase (30 to 120 seconds): Alternating, synchronous bursts of muscular contraction and relaxation. Manifests as rhythmic, violent bilaterally symmetrical jerking, accompanied by massive autonomic discharge: tachycardia, hypertension, diaphoresis, pupillary dilation, and excessive hypersalivation.
4. Postictal Phase (Minutes to Hours): Flaccid muscular relaxation, deep stertorous respirations (compensating for profound lactic acidosis), confusion, lethargy, headache, and gradual return of orientation. Paramedics may observe transient focal weakness (Todd's Paresis), which resolves within 24 to 48 hours and must not be confused with acute stroke.

Status Epilepticus: Definition and Cellular Emergency

Status Epilepticus (SE) is defined by the International League Against Epilepsy (ILAE) and Canadian emergency standards as:

• Continuous, unremitting seizure activity lasting >= 5 minutes, OR
• Two or more distinct discrete seizures without full recovery of consciousness between episodes.

Pathophysiological Timeline of Status Epilepticus:
- Phase 1 (0–30 minutes): Compensatory hyperadrenergic surge, massive catecholamine release, tachycardia, hypertension, hyperglycemia, hyperthermia. Cerebral blood flow increases to match astronomical neuronal metabolic demand.
- Phase 2 (>30–60 minutes): Cellular decompensation. Excitotoxicity: sustained glutamate release activates NMDA receptors, causing toxic intracellular calcium overload, mitochondrial failure, and neuronal apoptosis. Systemic collapse ensues: hyperthermia, severe lactic and respiratory acidosis, rhabdomyolysis, hyperkalemia, pulmonary edema, and refractory hypotension.

Status epilepticus is a medical emergency with up to a 20% adult mortality rate. Neuronal death begins after 5 minutes of continuous convulsive activity, dictating immediate prehospital termination.

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Prehospital Management of Status Epilepticus & Reversible Causes

Primary care paramedic care during active seizures focuses on immediate threat mitigation:

1. Patient Safety & Positioning: Clear hard or sharp objects from the surroundings. Place padding beneath the head. Do NOT forcefully restrain extremities, and NEVER insert any object, bite block, or fingers into the patient's mouth (which causes severe dental trauma and airway obstruction).
2. Airway & High-Flow Oxygen: Following cessation of active convulsion, immediately place the patient into the lateral recovery position to allow oral secretions and vomitus to drain gravitationally. Suction the oropharynx gently as needed. Apply high-flow oxygen via non-rebreather mask (12–15 L/min) or provide bag-valve-mask ventilations with an NPA if postictal respiratory depression occurs.
3. Investigating Reversible Triggers: Primary care paramedics systematically rule out life-threatening secondary causes:
   • Hypoglycemia: Mandatory immediate capillary blood glucose check (administer IV dextrose or IM glucagon if <4.0 mmol/L).
   • Hypoxia: Pulse oximetry and airway assessment.
   • Eclampsia: In any female of childbearing age (>20 weeks gestation up to 6 weeks postpartum) presenting with seizures and hypertension, suspect eclampsia (first-line treatment is magnesium sulfate via ALS intercept).
   • Toxicology: Check for pill bottles, toxic ingestions (tramadol, bupropion, tricyclic antidepressants, isoniazid), or acute alcohol/benzodiazepine withdrawal.
   • Trauma & Infection: Evaluate for occult head trauma or meningeal signs (fever, purpuric rash, nuchal rigidity).
4. Pharmacological Termination: In Canadian paramedic systems, convulsive status epilepticus lasting >= 5 minutes warrants immediate benzodiazepine administration (e.g., Midazolam 10 mg IM/IN or 5 mg IV, Lorazepam, or Diazepam) under regional ALS protocols or PCP extended scopes.

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Clinical Scenario: Acute MCA Occlusion with Field EVT Bypass

A 71-year-old female is found sitting on her living room couch by her daughter, slumped to the left side and unable to speak. The daughter confirms she was talking on the phone with her mother 45 minutes prior and she was completely normal.

1. Rapid Primary Exam & Stroke Screen: Paramedics arrive at 10:15. Airway is patent, breathing normal, pulse 88 bpm irregular (atrial fibrillation). Assessment reveals right-sided facial paralysis, total flaccidity of the right arm with no antigravity effort, no grip strength on the right, and global expressive aphasia.
2. LVO Calculation: The paramedic calculates the LAMS score: Facial droop (1) + Arm drift falls rapidly (2) + Grip strength no grip (2) = LAMS Score 5/5, confirming a high probability of a dominant Left Middle Cerebral Artery (M1) occlusion.
3. Time Verification & Glucometry: Capillary blood glucose is 6.2 mmol/L (ruling out hypoglycemia). Last Seen Normal is confirmed with the daughter at 09:30 (elapsed time 45 minutes).
4. Transport Decision: The regional primary community hospital is 8 minutes away, but the regional Comprehensive Stroke Centre (with EVT capabilities) is 24 minutes away. Meeting local bypass criteria (LAMS >= 4, LSN <6 hours, blood glucose normal), the crew initiates direct Comprehensive Stroke Bypass.
5. En-Route Care & Pre-Notification: Vital signs show BP 196/104 mmHg. The paramedic avoids any blood pressure reduction, keeping the head of the stretcher elevated 30 degrees to optimize venous drainage while preserving cerebral perfusion. A direct 'Stroke Code EVT' pre-alert is transmitted to the comprehensive team. The patient is transported directly onto the CT scanner bed upon arrival, where neuroimaging confirms an M1 occlusion successfully revascularized via endovascular thrombectomy.