Comprehensive Nursing Neurology and Cerebrovascular Accident (CVA) Study Guide

Comprehensive practice flashcards covering cerebrovascular accidents (CVA), neuroanatomy, cranial nerve assessments, increased ICP management, head trauma, spinal cord injuries, seizure disorders, infectious neurological diseases, and brain death criteria.

How many neurons die each minute without treatment during an acute stroke, illustrating the concept 'Time is Brain'?

Approximately $1.9\text{ million}$ neurons die each minute.

What are the two major classifications of stroke and their relative percentages of incidence?

Ischemic stroke ($87\%$ of all strokes) and hemorrhagic stroke ($13\%$ of all strokes).

How do thrombotic and embolic ischemic strokes differ in etiology and typical onset?

Thrombotic strokes occur when a blood clot forms directly within a brain artery (commonly from atherosclerosis), featuring a slower onset and possible TIA history. Embolic strokes occur when a clot travels from elsewhere (usually the heart, with atrial fibrillation being the #1 cause), featuring a sudden onset.

What is the hallmark symptom and common cause of a subarachnoid hemorrhage (SAH)?

A sudden, thunderclap headache described as the 'worst headache of my life,' commonly caused by the rupture of a cerebral aneurysm between the arachnoid and pia mater.

What are the defining characteristics of a Transient Ischemic Attack (TIA) and its prognostic significance?

A TIA involves temporary neurological dysfunction lasting $<24\text{ hours}$ (usually $<1\text{ hour}$) with complete symptom resolution and no permanent brain damage; however, $10\text{--}15\%$ of TIA patients suffer a stroke within $3\text{ months}$.

What is the #1 modifiable risk factor for all types of stroke?

Hypertension.

What clinical assessment does each letter represent in the BE-FAST stroke recognition tool?

B: Balance (sudden loss of balance/coordination); E: Eyes (sudden vision changes/loss); F: Face (facial drooping); A: Arms (arm weakness/drift); S: Speech (slurred, strange, or unable to speak); T: Time (call 911 immediately and note time of symptom onset).

What is the administration time window and prerequisite diagnostic imaging for tissue plasminogen activator (tPA) in ischemic stroke?

tPA must be administered within $3\text{--}4.5\text{ hours}$ of symptom onset, and a non-contrast CT scan must be performed first to rule out hemorrhagic stroke.

What are key absolute contraindications for receiving tPA in acute ischemic stroke?

Hemorrhagic stroke, recent surgery ($<14\text{ days}$), recent head trauma, active internal bleeding, uncontrolled hypertension ($\text{BP} > 185/110\text{ mmHg}$), recent stroke within $3\text{ months}$, certain anticoagulants, platelet count $<100,000$, or blood glucose $<50\text{ mg/dL}$ or $>400\text{ mg/dL}$.

What vital sign parameters and monitoring intervals are mandated following tPA administration?

Vital signs and neuro checks every $15\text{ minutes}$ for the first $2\text{ hours}$, then every $30\text{ minutes}$ for $6\text{ hours}$, then hourly for $16\text{ hours}$, keeping blood pressure strictly $<180/105\text{ mmHg}$.

Why is permissive hypertension up to $220/120\text{ mmHg}$ allowed in acute ischemic stroke patients who do not receive tPA?

Higher blood pressure helps force perfusion through collateral vessels to preserve ischemic brain tissue.

How do left hemisphere and right hemisphere stroke manifestations differ regarding speech and behavior?

Left hemisphere strokes cause right-sided motor deficits, aphasia, reading/writing difficulties, and slow, cautious behavior with depression. Right hemisphere strokes cause left-sided motor deficits, left neglect, spatial-perceptual deficits, and impulsive behavior with denial of deficits.

How do Broca's and Wernicke's aphasia differ in expression, comprehension, and cerebral location?

Broca's (expressive) aphasia is located in the frontal lobe; speech is non-fluent and telegraphic with intact comprehension. Wernicke's (receptive) aphasia is located in the temporal lobe; speech is fluent but nonsensical ('word salad') with impaired comprehension.

What medication is specifically administered following a subarachnoid hemorrhage (SAH) to prevent vasospasm?

Nimodipine (a calcium channel blocker).

What neurotransmitters are utilized preganglionically and postganglionically in the sympathetic (SNS) versus parasympathetic (PNS) nervous systems?

Both SNS and PNS utilize Acetylcholine (ACh) as their preganglionic neurotransmitter. Postganglionically, the SNS utilizes Norepinephrine (NE) (except at the adrenal medulla, which secretes epinephrine into the blood), whereas the PNS utilizes Acetylcholine (ACh).

What are the primary excitatory and inhibitory neurotransmitters in the central nervous system?

Glutamate is the primary excitatory neurotransmitter; GABA is the primary inhibitory neurotransmitter.

Why do cerebellar lesions cause ipsilateral motor deficits, whereas cerebral cortical lesions cause contralateral deficits?

Motor and sensory pathways decussate (cross) in the brainstem and spinal cord causing contralateral deficits for cerebral injuries, whereas cerebellar pathways do not cross in the same manner and cause same-side (ipsilateral) deficits.

Which two cranial nerves are responsible for the gag reflex, and what is the primary nursing safety implication if they are impaired?

Cranial nerves IX (Glossopharyngeal) and X (Vagus); if impaired, the patient is at severe risk for aspiration and must remain NPO until formal swallowing evaluation is completed.

What life-threatening pathology is signaled by a newly developed unilateral fixed, dilated pupil?

Compression of Cranial Nerve III (Oculomotor), which is a critical sign of impending brain herniation.

Which cranial nerves are essential for corneal protection, and what interventions are indicated when they are damaged?

Cranial Nerve V (Trigeminal, sensory) and Cranial Nerve VII (Facial, motor closure); interventions include lubricating eye drops, ophthalmic ointment, moisture chamber goggles, or taping the eyes shut to prevent corneal drying and ulceration.

What physical responses does the mnemonic SLUDGE describe in the context of cholinergic agonist stimulation?

Salivation, Lacrimation, Urination, Defecation, GI upset, and Emesis.

What is the clinical significance of a positive Babinski reflex in an adult versus an infant under $2\text{ years}$ of age?

In an infant under $2\text{ years}$, toe extension and fanning is normal due to incomplete myelination; in an adult, a positive Babinski reflex indicates an upper motor neuron (UMN) lesion in the brain or spinal cord.

What are the three response categories and total score boundaries on the Glasgow Coma Scale (GCS)?

Eye opening ($1\text{--}4$ points), Verbal response ($1\text{--}5$ points), and Motor response ($1\text{--}6$ points), yielding total scores from $3$ (lowest/flaccid) to $15$ (fully conscious).

How do decorticate and decerebrate posturing appear, and what do they indicate regarding brain dysfunction?

Decorticate posturing features abnormal flexion of arms toward the chest ('core') with legs extended, indicating cerebral cortex dysfunction; decerebrate posturing features stiff abnormal extension of both arms and legs, indicating entire cerebrum/brainstem dysfunction and carrying a worse prognosis.

What three clinical signs constitute Cushing's Triad, and what does its presence indicate?

1. Increased systolic blood pressure (with widened pulse pressure); 2. Decreased heart rate (bradycardia); 3. Irregular respirations. It is a late, grave sign of severely increased intracranial pressure (ICP) indicating imminent herniation.

What is the formula and target therapeutic range for Cerebral Perfusion Pressure (CPP)?

$\text{CPP} = \text{MAP} - \text{ICP}$, with a normal range of $70\text{--}100\text{ mmHg}$; cerebral ischemia begins when $\text{CPP} < 50\text{ mmHg}$.

Why is a lumbar puncture strictly contraindicated when a patient has suspected increased ICP?

Sudden decompression of cerebrospinal fluid pressure from the spinal canal can cause rapid downward herniation of brain tissue, resulting in brainstem compression and death.

Why is mild hyperventilation to lower $\text{CO}_2$ used as a temporary emergency intervention for elevated ICP?

$\text{CO}_2$ is a potent cerebral vasodilator; keeping $\text{CO}_2$ slightly low causes cerebral vasoconstriction, reducing intracranial blood volume and lowering ICP.

What are the classic physical signs of a basilar skull fracture?

Battle's sign (bruising behind the ear), raccoon eyes (periorbital ecchymosis), CSF rhinorrhea (leakage from nose), and CSF otorrhea (leakage from ears).

How do epidural hematomas and subdural hematomas differ in source of bleeding, speed of onset, and classic clinical course?

Epidural hematomas involve rapid arterial bleeding (middle meningeal artery) characterized by initial loss of consciousness, a temporary lucid interval, and rapid deterioration (a surgical emergency). Subdural hematomas involve slower venous bleeding between the dura and arachnoid, presenting as acute ($<48\text{ hours}$), subacute ($48\text{ hours to } 2\text{ weeks}$), or chronic.

Why do elderly patients have a higher risk of presenting late with chronic subdural hematomas after minor falls?

Age-related brain atrophy ($10\text{--}20\%$ volume loss by the 80s) leaves more space in the skull for venous blood to accumulate before ICP rises, while bridging veins are stretched and tear more easily from minor trauma.

What distinguishes simple partial seizures from complex partial seizures?

Simple partial seizures do not cause a loss of consciousness (presenting with focal motor or sensory phenomena); complex partial seizures (commonly in the temporal lobe) involve altered consciousness and automatisms (e.g., lip smacking, clothes picking) followed by post-ictal confusion.

Why is status epilepticus ($\ge 30\text{--}60\text{ minutes}$ of seizure activity) a life-threatening emergency?

Continuous widespread neuronal firing rapidly exhausts the brain's glucose stores, precipitating anaerobic metabolism, cerebral ischemia, and irreversible brain damage.

What is the therapeutic serum level of phenytoin (Dilantin), and what is a classic adverse effect associated with oral tissue?

The therapeutic range is $10\text{--}20\text{ mcg/mL}$, and a classic adverse effect is gingival hyperplasia (overgrowth of the gums).

What level of spinal cord injury causes total loss of respiratory function requiring mechanical ventilator dependence?

Spinal cord injury above the $C_4$ level.

What is Autonomic Dysreflexia, what levels of spinal cord injury are susceptible, and what are its classic manifestations?

An exaggerated, uninhibited sympathetic response to a noxious stimulus below the level of injury in patients with SCI at or above $T_6$, manifested by severe pounding headache, profuse sweating and piloerection above the lesion, severe hypertension, and reflex bradycardia.

What are the priority emergency nursing actions for Autonomic Dysreflexia, in sequence?

1. Immediately elevate the head of the bed (HOB) to lower blood pressure; 2. Identify and eliminate the noxious trigger (check for bladder distension/kinked Foley, fecal impaction, skin pressure, tight clothing); 3. Administer antihypertensive medications if BP remains elevated (never give beta-blockers due to baseline bradycardia).

How do spinal shock and neurogenic shock differ clinically?

Spinal shock is a temporary loss of spinal reflex and motor/sensory function below the lesion causing flaccid paralysis without circulatory collapse; neurogenic shock is a true hemodynamic shock state caused by loss of sympathetic vasomotor tone, characterized by hypotension, bradycardia, and warm, dry skin.

What are the definitions of Kernig's sign and Brudzinski's sign in bacterial meningitis?

Kernig's sign: Inability to extend the knee when the hip is flexed to $90^\circ$ due to severe hamstring stiffness. Brudzinski's sign: Passive flexion of the neck triggers involuntary flexion of the hips and knees.

What is the time threshold for administering antibiotics in suspected bacterial meningitis, and what medication is given immediately beforehand?

Broad-spectrum IV antibiotics must be administered within $30\text{ minutes}$ of hospital arrival; Dexamethasone (Decadron) is given $15\text{--}20\text{ minutes}$ before the first dose of antibiotics.

What is the critical clinical distinction between meningitis and encephalitis?

In meningitis, brain tissue is spared and cerebral function is largely normal despite meningeal irritation and fever; in encephalitis, the brain parenchyma itself is inflamed, causing abnormal brain function (hemiparesis, tremors, speech deficits, memory impairment, coma).

How do Myasthenic Crisis and Cholinergic Crisis differ in underlying cause, pupil appearance, and SLUDGE features?

Myasthenic crisis is caused by worsening disease/insufficient acetylcholine, presenting with normal pupils and absent SLUDGE signs. Cholinergic crisis is caused by overmedication with acetylcholinesterase inhibitors, presenting with pinpoint pupils (miosis) and active SLUDGE signs (excessive secretions, diarrhea, urination).

What are the three cardinal clinical signs required to confirm brain death?

1. Coma/complete unresponsiveness; 2. Complete absence of all brainstem reflexes (gag, cough, corneal, pupillary, caloric); 3. Apnea (lack of spontaneous respirations during formal apnea testing).