6.1 Neurological Assessment & Stroke Care

6.1 Neurological Assessment & Stroke Care

Neurological assessment demands systematic evaluation, acute pattern recognition, and rapid intervention. Because nervous tissue possesses negligible cellular glycogen reserves and tolerates ischemia poorly, subtle alterations in neurological status frequently represent critical medical emergencies. Registered nurses practicing within acute medical-surgical and critical care settings must master objective clinical scoring, cerebral hemodynamics, acute neurovascular syndromes, and emergency seizure management.

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Comprehensive Neurological Assessment

The fundamental cornerstone of neurological nursing is the continuous assessment of the central and peripheral nervous systems. Clinicians must establish a dependable baseline against which all subsequent assessments are compared.

Level of Consciousness (LOC)

Level of consciousness is the single most sensitive, reliable indicator of neurological deterioration. Alterations in cortical perfusion or metabolic equilibrium manifest first as subtle behavioral changes—restlessness, agitation, anxiety, disorientation, or delayed processing—long before focal motor deficits or autonomic pupillary abnormalities appear. When evaluating consciousness, clinicians distinguish between:

• Arousal (Wakefulness): Mediated anatomically by the ascending reticular activating system (ARAS) in the brainstem; assessed by the patient's response to verbal, tactile, or noxious stimuli.
• Awareness (Content of Consciousness): Mediated by higher cerebral cortical networks; assessed through orientation to person, place, time, and clinical situation, as well as cognitive reasoning and command-following.

The Glasgow Coma Scale (GCS)

Originally developed in 1974, the Glasgow Coma Scale provides a standardized, objective framework for quantifying depth of consciousness across three distinct behavioural parameters: Eye Opening (E), Verbal Response (V), and Motor Response (M). Total scores range from a minimum of 3 (profound coma or brain death) to a maximum of 15 (fully awake, alert, and oriented).

Cranial Nerve Examination Basics

A focused cranial nerve assessment evaluates brainstem integrity:

• CN II (Optic) & CN III (Oculomotor): Pupillary light reflex. The optic nerve transmits the afferent light impulse to the midbrain; the oculomotor nerve delivers the parasympathetic efferent impulse to constrict the iris sphincter. Normal pupils are equal, round, and briskly reactive to light (PERRLA, 2-5 mm in diameter). A unilaterally dilated, non-reactive (blown) pupil indicates uncal herniation compressing the ipsilateral CN III against the tentorium cerebelli.
• CN III, IV (Trochlear), & VI (Abducens): Extraocular muscle movements. Impairment produces diplopia, dysconjugate gaze, or nystagmus.
• CN V (Trigeminal) & CN VII (Facial): Corneal reflex (protective blink response to tactile cornea stimulation) and symmetric facial muscle expression (evaluating facial droop in acute stroke).
• CN IX (Glossopharyngeal) & CN X (Vagus): Bilateral elevation of the soft palate, symmetric uvula rise, phonation, and the protective pharyngeal gag and swallow reflexes.
• CN XI (Spinal Accessory) & CN XII (Hypoglossal): Shoulder shrug against resistance and midline tongue protrusion without deviation.

Motor Function and Pathological Posturing

Motor strength is graded bilaterally from 0 (complete flaccid paralysis) to 5 (full active range of motion against maximum resistance). When cortical inhibition is compromised by severe intracranial pathology, distinct pathological motor postures emerge in response to pain:

• Decorticate Posturing (Abnormal Flexion, Score = 3): Characterized by rigid flexion of the arms, wrists, and fingers held tightly against the chest ("core"), with adducted upper extremities and extended, internally rotated lower extremities with plantar flexion. This sign reflects destructive lesions of the cerebral cortex or corticospinal tracts above the level of the brainstem (diencephalon/subcortical white matter).
• Decerebrate Posturing (Abnormal Extension, Score = 2): Characterized by rigid extension, adduction, and hyperpronation of the upper extremities with clenched teeth, extended neck, and rigid extension of the legs with plantar flexion. This posture signifies advanced destructive lesions of the midbrain and upper pons (brainstem damage). Decerebrate posturing indicates greater neurological deterioration and a poorer prognosis than decorticate posturing.

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Increased Intracranial Pressure (ICP) and Cerebral Dynamics

The intracranial vault is an inflexible anatomical compartment governed by strict volumetric relationships and hydrodynamic pressures.

The Monro-Kellie Hypothesis and Intracranial Compliance

The Monro-Kellie hypothesis states that the cranial vault is a rigid, non-distensible bone container with a fixed internal volume consisting of three components:

1. Brain tissue and parenchymal interstitial water: ~80% of volume
2. Intravascular blood (venous and arterial): ~10% of volume
3. Cerebrospinal fluid (CSF): ~10% of volume

Because the total cranial volume is unyielding, the sum of these volumes must remain constant: Brain Volume + Blood Volume + CSF Volume = Intracranial Volume. If any single component increases in volume (e.g., cerebral edema, intracranial hemorrhage, tumor) or an abnormal space-occupying lesion develops, reciprocal compensatory displacement of the other components must occur to preserve normal pressure. CSF is displaced into the spinal subarachnoid space and reabsorption is accelerated; venous blood is shunted into the internal jugular veins. Once these compensatory mechanisms are exhausted, intracranial compliance is lost, and even minuscule additions of volume produce steep, exponential rises in intracranial pressure.

Cerebral Perfusion Pressure (CPP)

Intracranial pressure in a resting, supine adult normally measures 5 to 15 mmHg. Sustained pressures exceeding 20 mmHg are pathological and require aggressive clinical intervention. Elevated ICP directly impairs cerebral perfusion, defined mathematically by the Cerebral Perfusion Pressure (CPP) equation:

CPP = MAP - ICP

Where Mean Arterial Pressure (MAP) is calculated as:

MAP = (Systolic BP + 2 * Diastolic BP) / 3

The physiological target for CPP in adults with severe brain injury or acute neurological compromise is 60 to 70 mmHg. A CPP below 50 mmHg results in cerebral hypoperfusion, severe cellular ischemia, and neuronal death, whereas a CPP below 30 mmHg produces irreversible cellular infarction. Conversely, driving CPP above 70-80 mmHg with excessive vasopressors increases the risk of acute respiratory distress syndrome (ARDS) and hyperperfusion-induced vasogenic edema.

Clinical Manifestations: Early Signs vs. Late Signs

Recognizing the progressive trajectory of intracranial hypertension prevents irreversible brainstem herniation:

• Early Manifestations: Subtle deterioration in LOC (restlessness, apathy, slight confusion), persistent dull headache that worsens upon awakening or coughing, blurred vision, diplopia, sluggish pupillary response to light, and nausea with intermittent vomiting (which may occur without preceding nausea).
• Late Manifestations: Profound stupor progressing to coma, fixed and dilated pupils, papilledema (optic disc swelling on funduscopic exam), motor weakness progressing to hemiplegia, decorticate or decerebrate posturing, and autonomic collapse known as Cushing's Triad.

Cushing's Triad vs. Shock Hemodynamics

Cushing's Triad is a late, ominous physiological response to severe brainstem ischemia and impending fatal cerebellar or uncal herniation. It occurs when swelling compresses brainstem vasomotor and cardiac centers, triggering massive sympathetic discharge followed by vagal parasympathetic baroreceptor activation. Clinicians must recognize that Cushing's Triad presents with hemodynamic parameters directly opposite to hypovolemic shock:

Evidence-Based Nursing Management of Increased ICP

Therapeutic nursing interventions focus on optimizing cerebral venous drainage, reducing cerebral metabolic demands, and avoiding sudden spikes in intrathoracic or intra-abdominal pressure:

• Patient Positioning: Maintain the head of the bed (HOB) elevated at 30 degrees with the neck in a neutral, midline position. This promotes passive venous return through the internal jugular veins. Avoid extreme neck rotation, hyperextension, or acute flexion, which compress jugular drainage. Avoid extreme hip flexion (>90 degrees), which elevates intra-abdominal pressure and impedes inferior vena cava and thoracic venous emptying.
• Activity Pacing and Environmental Control: Avoid clustering multiple stressful nursing interventions (e.g., bathing, linen changes, endotracheal suctioning) together, as cumulative stimuli induce sustained ICP spikes. Provide a quiet, dimly lit, stress-free environment; limit visitor stimulation.
• Airway Clearance and Ventilation: Endotracheal suctioning triggers coughing, bronchospasm, and sharp elevations in intrathoracic and intracranial pressure. Always pre-oxygenate with 100% O2 prior to suctioning, limit each suction pass to fewer than 10 seconds, restrict attempts to a maximum of two passes per episode, and never perform routine, scheduled suctioning without clear clinical indications (e.g., adventitious breath sounds, visible secretions).
• Ventilatory Targets (PaCO2 Regulation): Arterial carbon dioxide (PaCO2) is a potent physiological regulator of cerebral blood flow. Elevated PaCO2 (>45 mmHg) induces pronounced cerebral arterial vasodilation, increasing intracranial blood volume and elevating ICP. Conversely, severe hypocapnia (PaCO2 <30 mmHg) causes extreme vasoconstriction, precipitating critical cerebral ischemia. Modern neurocritical care guidelines mandate maintaining normocapnia with PaCO2 at 35 to 40 mmHg. Prophylactic hyperventilation is strictly contraindicated; transient hyperventilation (PaCO2 30-35 mmHg) is reserved exclusively as a temporary bridge during acute, catastrophic herniation while preparing definitive surgical or hyperosmolar interventions.
• Hyperosmolar Pharmacotherapy:
  • Mannitol (20% or 25% IV infusion): An osmotic diuretic that expands intravascular volume, reduces blood viscosity, and creates an osmotic gradient drawing water from edematous parenchymal brain tissue into the vascular space for renal elimination. Administer via an IV line equipped with an in-line filter to capture microscopic crystals. Monitor serum osmolality closely (hold if serum osmolality exceeds 320 mOsm/kg to avoid acute renal failure) and ensure adequate fluid volume replacement to prevent hypovolemic hypotension.
  • Hypertonic Saline: Draws water from brain tissue into the circulation. Access depends on concentration and protocol:3%saline may use appropriate central or closely monitored large peripheral access; follow the specified access requirements for more concentrated solutions. Check sodium every 4–6 hours and monitor fluid balance, renal function and the infusion site. Avoid severe hypernatremia and excessive correction of pre-existing hyponatremia; use the prescribed sodium target and correction limits.
• Normothermia and Sedation: Fever accelerates cerebral metabolic rate of oxygen consumption (CMRO2) by 7-10% for every 1°C increase, exacerbating neuronal ischemia. Maintain strict normothermia (36.0-37.0°C) using antipyretics and targeted temperature management cooling devices. Control shivering, pain, and agitation using titrated IV analgesics (fentanyl) and sedatives (propofol or dexmedetomidine).

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Acute Stroke Management

Stroke represents a sudden focal neurological deficit caused by cerebrovascular occlusion or hemorrhage. Time is brain: approximately 1.9 million neurons are lost every minute an ischemic stroke remains untreated.

Ischemic vs. Hemorrhagic Stroke

• Ischemic Stroke (~87% of all cases): Caused by sudden arterial occlusion secondary to a local thrombus (atherosclerotic disease) or an embolus (commonly originating from the left atrium in atrial fibrillation or carotid plaque rupture). The ischemic zone consists of a central, non-viable core of infarcted tissue surrounded by the ischemic penumbra—a zone of hypoperfused, metabolically compromised tissue that remains salvageable if reperfusion is achieved swiftly.
• Hemorrhagic Stroke (~13% of cases): Arises from vascular rupture, categorized as Intracerebral Hemorrhage (ICH) (spontaneous rupture of small penetrating vessels driven by chronic hypertension or amyloid angiopathy) or Subarachnoid Hemorrhage (SAH) (extravasation of blood into the subarachnoid space, most commonly from a ruptured saccular intracranial berry aneurysm or arteriovenous malformation [AVM]). SAH classically presents with a sudden, devastating "thunderclap" headache described as "the worst headache of my life," accompanied by meningismus (nuchal rigidity, photophobia, positive Kernig's and Brudzinski's signs).

Rapid Prehospital and Emergency Triage: The FAST Algorithm

The FAST assessment tool facilitates rapid recognition by clinicians and the public:

• F - Face: Ask patient to smile or show teeth; observe for unilateral facial droop.
• A - Arms: Ask patient to extend both arms forward at 90 degrees (sitting) or 45 degrees (supine) with eyes closed for 10 seconds; observe for downward drift or pronation of one arm.
• S - Speech: Ask patient to repeat a standard phrase (e.g., "You can't teach an old dog new tricks"); listen for slurred speech (dysarthria) or word-finding difficulty/aphasia.
• T - Time: Determine the exact Last Known Normal (LKN) or "last known well" time. If the patient awakens with neurological deficits (wake-up stroke), LKN is defined as the time the patient was last observed symptom-free before going to sleep.

Diagnostic Neuroimaging: The Non-Contrast Head CT

Upon emergency department arrival, the immediate diagnostic imperative is a stat non-contrast computed tomography (NCCT) scan of the head, completed within 20 minutes of door arrival. The primary purpose of the non-contrast CT is not to verify ischemia (early ischemic changes may be subtle or undetectable in the first few hours), but to definitively exclude intracranial hemorrhage. The presence of hyperdense acute blood on CT immediately disqualifies the patient from receiving thrombolytic therapy and shifts clinical management to hemorrhagic neurosurgical pathways.

Intravenous Thrombolysis (rtPA / Alteplase / Tenecteplase)

Recombinant tissue plasminogen activator (rtPA / alteplase) converts plasminogen to plasmin, degrading fibrin clots and restoring microvascular blood flow to the ischemic penumbra.

Therapeutic Window

For eligible adults with disabling ischemic stroke, current AHA/ASA guidance recommends alteplase or tenecteplase as soon as possible within 4.5 hours of onset/last known well. Selected patients with unknown onset or 4.5–9 hours from onset may qualify using advanced-imaging criteria. Age over 80, prior stroke with diabetes, or a high NIHSS score alone must not be used as automatic exclusions. Follow the current stroke-team protocol rather than the older ECASS 3 trial exclusions.

Blood Pressure Parameters for Thrombolysis

Uncontrolled hypertension during or after thrombolysis drastically increases the risk of fatal symptomatic intracranial hemorrhage (sICH):

• Pre-treatment Threshold: Blood pressure must be reduced to Systolic BP <185 mmHg and Diastolic BP <110 mmHg prior to initiating alteplase. IV antihypertensives of choice include labetalol (10-20 mg IV push over 1-2 min, may repeat once) or nicardipine continuous infusion (5 mg/h, titrated up to 15 mg/h).
• Post-treatment Threshold: Blood pressure must be maintained below Systolic BP <180 mmHg and Diastolic BP <105 mmHg for at least 24 hours following completion of the thrombolytic infusion.

Contraindications and Specialist Risk Assessment

Use the current stroke-team checklist; distinguish absolute exclusions from situations requiring individual risk assessment:

• Do not give IV thrombolysis with intracranial hemorrhage on CT, suspected subarachnoid hemorrhage, or active internal bleeding.
• Platelets<100,000/mm³, INR>1.7, PT>15 seconds or aPTT>40 seconds preclude treatment. Review all anticoagulant exposure, including therapeutic LMWH within 24 hours and recent DOAC use, with the stroke team.
• Recent intracranial/spinal surgery or significant head/spinal injury requires urgent specialist review. CNS surgery within 14 days precludes IVT; surgery 14 days to 3 months earlier may be considered individually.
• Recent major non-CNS surgery, major trauma or treated GI/GU bleeding requires an individualized benefit–risk decision with the relevant specialists. Major non-CNS surgery within 10 days is a relative contraindication, not an automatic absolute exclusion.
• Correct glucose<50 mg/dL promptly, then reassess the deficit and thrombolysis eligibility.

Nursing Surveillance During and After Thrombolysis

• Give the prescribed agent: alteplase 0.9 mg/kg (maximum 90 mg),10%as a 1-minute IV bolus and 90%over 60 minutes; or tenecteplase 0.25 mg/kg (maximum 25 mg) as a single IV bolus. Verify the agent, formulation and stroke protocol.
• Conduct vital signs and neurological checks (using the NIH Stroke Scale): every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, and every 1 hour for the remaining 16 hours.
• Avoid inserting invasive lines (nasogastric tubes, indwelling foley catheters, arterial lines, central venous lines) for 24 hours post-infusion unless clinically mandatory, due to hemorrhage risk.
• Discontinue the infusion immediately and obtain a stat non-contrast head CT if the patient develops signs of acute intracranial bleeding: sudden severe headache, acute severe hypertension, nausea/vomiting, or sudden deterioration in neurological score.
• Hold all antiplatelet (aspirin, clopidogrel) and anticoagulant medications for 24 hours following alteplase, pending a repeat non-contrast head CT confirming the absence of hemorrhage.

Hemorrhagic Stroke Precautions

For patients with confirmed intracerebral or subarachnoid hemorrhage:

• Use stroke-specific BP orders with smooth titration and frequent neurological checks. For acute spontaneous ICH presenting with SBP 150–220 mmHg, current AHA guidance supports reduction to 130–<140 mmHg while avoiding SBP<130. For unsecured aneurysmal SAH, avoid severe hypertension, hypotension and abrupt BP changes; the treating team individualizes the target rather than applying the ICH target automatically.
• Immediately reverse therapeutic anticoagulation: administer four-factor prothrombin complex concentrate (4F-PCC) and IV vitamin K for warfarin-associated hemorrhage; administer idarucizumab for dabigatran reversal; administer andexanet alfa for apixaban/rivaroxaban reversal.
• Initiate aneurysm precautions: bed rest in a quiet, dark, private room; avoid Valsalva maneuvers by administering stool softeners; avoid stimulants; administer prophylactic nimodipine (60 mg orally every 4 hours for 21 days) to prevent delayed cerebral vasospasm in subarachnoid hemorrhage.

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Seizure Precautions, Ictal Care, and Status Epilepticus

A seizure is an abrupt, abnormal, unregulated paroxysmal electrical discharge of cortical neurons. Epilepsy is a chronic neurological disorder characterized by recurrent unprovoked seizures, but acute symptomatic seizures frequently arise from electrolyte derangements (hyponatremia, hypocalcemia), acute alcohol or benzodiazepine withdrawal, hypoglycemia, stroke, head trauma, and CNS infections.

Stages of a Seizure

1. Aura / Pre-ictal Phase: A focal sensory, cognitive, or autonomic warning sign (e.g., epigastric rising sensation, olfactory hallucination of burning rubber, metallic taste, visual flashing lights, intense déjà vu) signaling the onset of electrical irritation.
2. Ictal Phase: The period of active, paroxysmal electrical seizure discharge:
   • Tonic Phase: Sudden loss of consciousness, sustained generalized muscular contraction, vocalization ("epileptic cry" from diaphragmatic spasm), cyanosis, and upward eye deviation.
   • Clonic Phase: Synchronous, bilateral, violent rhythmic jerking contractions alternating with muscular relaxation, hyperventilation, diaphoresis, and excessive salivation (frothing).
3. Post-ictal Phase: The recovery phase following seizure termination, characterized by deep somnolence, muscular flaccidity, confusion, headache, retrograde amnesia, and occasional transient focal weakness (Todd's paresis).

Bedside Seizure Precautions

For any patient with a seizure history, altered cerebral hemodynamics, or acute neurological injury, maintain the following precautions at the bedside:

• Padded side rails (all four rails padded with approved safety pads).
• Suction equipment connected, fully functional, and immediately reachable with Yankauer suction tips.
• Oxygen delivery equipment (cannula, non-rebreather mask) and bag-valve-mask (BVM) manual resuscitator present.
• Functioning, patent peripheral IV catheter maintained at all times.
• Bed positioned in the lowest height setting with wheels locked.

Nursing Actions During an Active Seizure

When a seizure occurs, the nurse's primary objectives are safety, airway preservation, and documentation:

1. Maintain Safety and Prevent Trauma: If the patient is sitting in a chair or standing, gently guide them down to the floor. Clear away hard, sharp, or hazardous furniture. Place a soft folded towel or pillow beneath the patient's head. Loosen tight clothing around the neck (neckties, collars).
2. Preserve Airway and Prevent Aspiration: Position the patient onto their side (lateral decubitus position) as soon as possible. This allows saliva, secretions, and vomitus to drain freely by gravity and prevents the relaxed tongue from occluding the hypopharynx.
3. DO NOT Force Anything into the Mouth: Never attempt to force a bite block, padded tongue blade, or airway adjunct into the patient's mouth during an active seizure. Forcing objects into clenched jaws fractures teeth, lacerates oral tissues, triggers vomiting, and creates aspirated foreign body airway obstruction.
4. DO NOT Restrain the Patient: Never attempt to hold down or physically restrain thrashing limbs. Restraining violent contractions causes musculoskeletal injuries, dislocations, and bone fractures.
5. Observe, Time, and Document: Note the exact time of onset and duration of each phase. Observe initial motor movements, direction of head and eye deviation, pupillary changes, presence of cyanosis, and autonomic signs. Monitor the post-ictal phase for time to recovery of consciousness.

Status Epilepticus Emergency Management

Status epilepticus is defined clinically as continuous seizure activity lasting >=5 minutes, or two or more distinct seizures occurring in rapid succession without the full recovery of consciousness between episodes. Prolonged seizure activity induces profound systemic and cerebral metabolic collapse: severe lactic acidosis, hyperthermia, rhabdomyolysis, hypoglycemia, hyperkalemia, cardiac arrhythmias, autonomic instability, and irreversible neuronal apoptosis from excitotoxicity.

Pharmacological Escalation Protocol for Status Epilepticus

• First-Line Therapy (Emergency Benzodiazepines, 0-10 minutes):
  • IV Lorazepam (Ativan): 0.1 mg/kg IV push (typically 4 mg administered at 2 mg/min); preferred due to prolonged CNS half-life. May repeat once after 5-10 minutes if seizures persist.
  • Alternative IV Diazepam (Valium): 5-10 mg IV push at 2-5 mg/min; rapid onset but redistributes rapidly into peripheral fat stores, requiring subsequent anti-seizure infusion.
  • IM Midazolam: 10 mg IM if IV access cannot be established immediately.
• Second-Line Therapy (Urgent Non-Sedating Antiseizure Infusions, 10-30 minutes):
  • IV Levetiracetam (Keppra): 60 mg/kg IV (up to 4,500 mg) infused over 10-15 minutes.
  • IV Fosphenytoin (Cerebyx): 20 mg PE (phenytoin equivalents)/kg IV infused at up to 150 mg PE/min with continuous ECG and blood pressure monitoring (eliminates the risk of purple glove syndrome and vehicle toxicity associated with classic phenytoin).
  • IV Sodium Valproate: 40 mg/kg IV infused over 10 minutes.
• Third-Line Therapy (Refractory Status Epilepticus, >30-60 minutes):
  • General anesthesia and continuous pharmacological burst suppression using continuous IV infusions of propofol, midazolam, or pentobarbital.
  • Mandates emergent endotracheal intubation, mechanical ventilation, invasive arterial pressure monitoring, and continuous bedside electroencephalographic (EEG) monitoring.