Neurology

The nervous system is the body’s command center, and when it fails the stakes are immediate — minutes decide the outcome of a stroke, and a rising pressure inside the skull can be lethal. This chapter walks the major neurologic emergencies and diseases: stroke, raised intracranial pressure, head and spinal trauma, seizures, and the slow diseases that erode the brain and nerves.

Section 1Stroke

Your brain is the hungriest organ you have. It makes up only about 2 percent of your body weight, yet it demands roughly 20 percent of your oxygen and glucose, and it has almost no way to store fuel of its own. That means brain tissue depends on a constant, second-by-second delivery of oxygen-rich blood through the carotid and vertebral arteries. When that delivery stops, neurons cannot switch to a backup plan the way muscle can. Within minutes they begin to fail, and soon after, they begin to die. A stroke (also called a cerebrovascular accident, or CVA) is exactly this: a sudden interruption of blood flow to part of the brain, causing that region to lose function.

Two ways the flow fails: ischemic vs hemorrhagic

There are two fundamentally different problems that can starve brain tissue, and telling them apart drives everything you do next. Explore the interactive figure below to see them side by side.

An ischemic stroke is a plumbing blockage. A vessel gets clogged and the tissue downstream is cut off. This is by far the most common type, making up about 87 percent of strokes. The clog comes in two flavors: a thrombotic stroke, where a clot forms right there on top of atherosclerotic plaque in a cerebral artery, and an embolic stroke, where a clot (often a fragment thrown from the heart during atrial fibrillation) travels through the bloodstream and lodges in a smaller brain vessel.

A hemorrhagic stroke is the opposite mechanism: a leak. A weakened or overstretched vessel ruptures and bleeds into or around the brain. Now there are two injuries happening at once. The tissue past the rupture is deprived of flow, and the escaping blood forms a mass that raises intracranial pressure and irritates surrounding tissue. Chronic hypertension and ruptured aneurysms are common culprits. Hemorrhagic strokes are less common but often more deadly.

The penumbra, and why time is brain

When an artery blocks, the tissue in the very center of the blocked zone dies quickly. But surrounding that dead core is a rim of tissue called the ischemic penumbra. These neurons are starving and silent, so they have stopped working, but they are not yet dead. They are being kept barely alive by trickles of blood from neighboring vessels. This penumbra is the whole reason we rush. If we can restore flow fast, penumbra neurons can wake back up and the deficit can shrink. If we wait, that salvageable rim converts into permanent dead tissue.

Clinicians estimate the brain loses roughly 1.9 million neurons every minute an ischemic stroke goes untreated. That staggering rate is the reason for the mantra time is brain. Every minute of delay is literally brain tissue you cannot get back.

Recognizing it fast: FAST

Because minutes matter, nurses and the public are taught a simple screen called FAST:

• F - Face: Ask the person to smile. Does one side droop?
• A - Arm: Ask them to raise both arms. Does one drift downward?
• S - Speech: Is speech slurred, absent, or strange? Can they repeat a simple sentence?
• T - Time: If any of these are present, note the time symptoms began and call for emergency help immediately.

That last letter is easy to gloss over but it may be the most important. Treatment eligibility depends entirely on knowing when the patient was last known well.

Why the CT scan comes before the clot-buster

The main clot-dissolving drug is tPA (tissue plasminogen activator, also called alteplase). It works beautifully on a clot, but it is a clot-dissolving (thrombolytic) drug. If the stroke were actually a bleed, giving tPA would pour fuel on a fire, dramatically worsening the hemorrhage. Here is the catch: ischemic and hemorrhagic strokes can look identical at the bedside. You cannot tell them apart by symptoms alone.

That is why an emergency non-contrast CT scan of the head is done first, every time. Its main job is to rule out a bleed. Only once blood is excluded can tPA be considered, and only within a strict window, usually within 3 to 4.5 hours of symptom onset for eligible patients. Some patients may also qualify for a mechanical thrombectomy, where the clot is physically pulled out, within a longer window.

Which side, which deficit

Because motor nerve tracts cross over in the lower medulla (the pyramidal decussation), a stroke on one side of the brain produces weakness on the opposite (contralateral) side of the body. A right-brain stroke causes left-sided weakness, and vice versa. Language adds another wrinkle: in most people the language centers live in the left hemisphere. So a left-brain stroke often produces aphasia, difficulty producing or understanding language, along with right-sided weakness. A right-brain stroke more often spares speech but may cause left-sided neglect, where the patient ignores their affected side entirely.

Section 2Raised intracranial pressure

Picture the brain as a delicate organ living inside a hard, sealed box: the skull. In a healthy person that box holds three things, and they share the space in a careful balance. There is the brain tissue itself (about 80% of the volume), the blood flowing through its vessels (about 10%), and the clear cerebrospinal fluid (CSF) that cushions and bathes it (about 10%). Because the skull cannot stretch, the total volume inside is fixed. The gentle pressure these three contents create is called the intracranial pressure (ICP), and normally it sits around 5 to 15 mmHg.

The Monro-Kellie doctrine: a box that cannot expand

The rule that governs all of this is the Monro-Kellie doctrine. It says that because the skull is a rigid, fixed container, the three volumes inside must add up to a constant. If one of them grows, another must shrink to make room, or the pressure will climb. At first the brain is clever about this. It buys time through compensation: it shunts CSF down into the spinal canal and squeezes some venous blood out of the skull. This is why a slowly growing problem can stay silent for a while. But this wiggle room is limited. Once those buffers are used up, even a tiny added volume causes the pressure to shoot up steeply. The patient falls off a compensation cliff, and small changes suddenly produce big, dangerous swings in ICP.

What raises the pressure

Anything that adds volume to that sealed box can raise ICP. The common culprits map neatly onto the three normal contents plus new intruders:

• Bleeding (hemorrhage) - an epidural, subdural, subarachnoid, or intracerebral bleed adds a pool of blood that takes up space.
• Tumor (mass lesion) - a growing mass literally crowds out brain, blood, and CSF.
• Cerebral edema - swelling of the brain tissue itself, often after trauma, stroke, or infection, as fluid leaks into or around cells.
• Hydrocephalus - a backup of CSF, either because too much is made, its flow is blocked, or it is not reabsorbed, so fluid accumulates in the ventricles.

The earliest warning: a change in consciousness

Here is the single most important nursing point. The earliest and most sensitive sign of rising ICP is a change in level of consciousness (LOC). The brain's alertness centers are exquisitely sensitive to pressure and to falling oxygen delivery. So before anything dramatic happens, the patient becomes subtly different: restless, confused, harder to rouse, more drowsy, slower to answer, or newly agitated. Families often notice it first ("she's just not herself"). Trust that. A dropping Glasgow Coma Scale (GCS) score is your red flag long before the classic textbook signs appear. Do not wait for pupils to change.

Cushing's triad: the late, ominous sign

When the pressure inside the skull rises high enough to threaten blood flow to the brainstem, the body launches a last-ditch rescue. To keep pushing blood past the crushing pressure, it drives the systolic blood pressure up. Baroreceptors sense that surging pressure and reflexively slow the heart, producing bradycardia. Meanwhile the pressure squeezes the brainstem's respiratory centers, making breathing irregular (for example, Cheyne-Stokes). Together these three make up Cushing's triad. It is a late and grave finding that signals the brainstem is in trouble.

Herniation: the feared end result

If the pressure is not relieved, the brain is forced across its normal partitions - under the falx, across the tentorial notch, or down through the foramen magnum at the skull's base. This shifting of brain tissue across its normal boundaries is called herniation. As tissue is pushed downward it crushes the brainstem, which controls breathing, heart rate, and consciousness. The results are catastrophic: a fixed, dilated pupil on the affected side (from cranial nerve III compression), loss of protective reflexes, respiratory arrest, and death. Herniation is the dreaded destination of untreated intracranial hypertension, and everything above is about catching the problem long before this point. Explore the figure below to see how a growing volume drives the pressure up and pushes the brain toward herniation.

Section 3Brain & spinal cord injury

Your brain is soft, delicate tissue floating inside a hard, unforgiving skull, cushioned by a thin layer of cerebrospinal fluid. That fluid normally acts like a shock absorber. But the skull that protects your brain from the outside world becomes a problem during trauma, because the brain can slam against the bone and there is nowhere for swelling to go. This is why head injuries are so dangerous: the box is sealed, and any extra blood or swelling raises pressure on the brain itself.

Concussion vs contusion, and the coup-contrecoup pattern

A concussion is a functional injury. The brain gets shaken hard enough to disrupt how neurons signal, but there is usually no visible bleeding or bruising on imaging. Patients often have a brief loss of consciousness, confusion, headache, and amnesia around the event. A contusion is a step worse: it is an actual bruise of brain tissue, with capillary bleeding and swelling you can often see on CT. Contusions can enlarge over hours, so serial neuro checks matter.

Both are frequently caused by a coup-contrecoup injury. Picture a moving head striking a dashboard. The brain first bruises directly under the point of impact (the coup), then rebounds and slams into the opposite side of the skull (the contrecoup). One blow, two injured areas.

Bleeding between the layers: epidural vs subdural hematoma

Three membranes wrap the brain: the tough outer dura mater, the middle arachnoid, and the delicate pia mater against the brain. Where the bleeding collects, and what vessel is torn, changes how fast the patient crashes.

An epidural hematoma is bleeding above the dura, classically from a torn middle meningeal artery after a temporal skull fracture. Because it is arterial, it fills fast under high pressure. The textbook picture is a lucid interval: the patient is knocked out, wakes up and seems fine, then rapidly deteriorates as the clot expands and compresses the brain. This is a neurosurgical emergency.

A subdural hematoma is bleeding below the dura, from torn bridging veins. Because it is venous, it oozes slowly, so symptoms can take hours, days, or even weeks to appear. It is especially common in older adults and people with chronic alcohol use, because brain atrophy stretches those bridging veins and makes them fragile.

Spinal cord injury by level

The spinal cord is the main data cable between brain and body. Where it is damaged determines what is lost below that point, because signals can no longer travel past the injury. As a rule, the higher the injury, the more of the body is affected.

• Lumbar/sacral injuries may affect the legs, bladder, and bowel.
• Thoracic injuries can cause paraplegia, loss of function in the legs and lower trunk.
• Cervical injuries can cause tetraplegia (quadriplegia), affecting all four limbs.

The scariest zone is the high cervical cord. The phrase students memorize is "C3, C4, C5 keep the diaphragm alive." The phrenic nerve, which drives the diaphragm, arises from these levels. An injury at or above C3-C5 can paralyze the diaphragm, so the patient cannot breathe on their own and needs immediate ventilatory support. Lower injuries are not off the hook: lesions from about C5 down through the upper thoracic cord knock out the intercostal and abdominal muscles, which shrinks vital capacity and weakens the cough even when the diaphragm still works, so secretions collect and respiratory failure can arrive days later. This is why airway and breathing come first in any suspected cervical injury, and why respiratory status is watched in cord injuries well below the neck.

Two shock states to keep straight

Spinal shock is the temporary loss of all reflexes, movement, and sensation below the injury right after trauma, a kind of neurological stunning that can last days to weeks. Neurogenic shock is a circulatory problem from losing sympathetic tone after a high injury, causing the classic triad of hypotension, bradycardia, and warm dry skin. Later, autonomic dysreflexia is a dangerous, exaggerated reflex in injuries at or above T6, usually triggered by a full bladder or bowel, causing a sudden dangerous spike in blood pressure that is a true emergency.

Explore the interactive figure below to see how these head injuries take shape.

Section 4Seizures & epilepsy

To understand a seizure, start with the normal brain. Your neurons are constantly talking to each other using tiny electrical signals, and in health that chatter is coordinated but not synchronized - different regions fire at different times for different jobs, like a huge orchestra where each section plays its own part. This balance is kept in check by a tug-of-war between excitatory signals (mostly the neurotransmitter glutamate, which says "fire") and inhibitory signals (mostly GABA, which says "settle down"). As long as that balance holds, the brain hums along smoothly.

A seizure is what happens when that balance breaks and a population of neurons suddenly fires all at once - a burst of abnormal, hypersynchronous electrical activity. Instead of the orchestra playing its parts, every instrument blasts the same note together. Depending on where in the brain this happens and how far it spreads, you get very different outward signs. One important distinction: a seizure is a single event, while epilepsy is a chronic condition defined by a tendency toward recurrent, unprovoked seizures (usually diagnosed after two or more, or one seizure plus a high risk of recurrence).

Focal vs. generalized: where the storm begins

Seizures are grouped by where the abnormal firing starts. A focal seizure (older term: partial) begins in one area of one hemisphere. Because only part of the brain is involved, the signs match that region - a twitching hand, an odd smell, a rising stomach sensation, or a period of staring and confusion. The person may stay aware (focal aware) or have altered awareness (focal impaired awareness). A focal seizure can sometimes spread and become generalized.

A generalized seizure begins in networks of both hemispheres at once. Awareness is usually impaired from the outset, though not always - in a myoclonic seizure the person stays fully aware through the sudden jerk, which is exactly why the current classification does not sort generalized seizures by awareness the way it sorts focal ones. The two you will see most often are tonic-clonic and absence.

In a tonic-clonic seizure you may also see cyanosis (breathing pauses during the tonic phase), tongue-biting, and loss of bladder control - all explained by whole-brain firing overriding normal muscle and autonomic control. Absence seizures are so brief they are often mistaken for daydreaming, which is why a child "not paying attention" in class sometimes turns out to be seizing dozens of times a day.

What sets a seizure off: common triggers

Anything that pushes the brain toward excitation - or removes something that was calming it - can lower the seizure threshold:

• Fever in young children - rapid temperature spikes cause febrile seizures, usually between 6 months and 5 years.
• Low sodium (hyponatremia) or low glucose (hypoglycemia) - neurons depend on stable electrolytes and fuel to control firing; when either drops, membranes become unstable.
• Missed antiseizure medication - the most common reason a person with epilepsy breaks through; the calming drug level falls too low.
• Alcohol withdrawal - alcohol suppresses the brain, so stopping abruptly leaves it in a rebound hyperexcitable state.
• Others: sleep deprivation, flashing lights, and infections such as meningitis.

Status epilepticus: the emergency

Status epilepticus is a seizure that lasts 5 minutes or longer, or repeated seizures without full recovery of consciousness in between. This is a true neurologic emergency. Prolonged firing burns through oxygen and glucose faster than the brain can supply them, and the sustained muscle activity drives up temperature and can injure neurons - leading to hypoxia, acidosis, and permanent damage. It requires rapid IV benzodiazepines (such as lorazepam) and airway support.

Nursing priorities during a seizure

Your job is protection, not intervention in the seizure itself - you cannot stop the electrical activity by hand, so focus on preventing injury:

• Protect the airway and head - turn the person to their side (recovery position) to let secretions drain and reduce aspiration risk; cushion the head and remove nearby hazards.
• Do not restrain - holding limbs down can cause fractures or dislocations; let the movements run their course.
• Nothing in the mouth - never insert objects or fingers; it risks broken teeth, bites, and airway blockage.
• Time it - note the start; if it reaches 5 minutes, treat as status epilepticus and get help.
• Stay and observe - loosen tight clothing, provide privacy, and document what you saw (movements, duration, incontinence) for the provider.

Section 5Neurodegenerative disease

Your brain runs on about 86 billion neurons, and here's the humbling part: for the most part, you were born with nearly all of them, and adult brains make very few new ones. Neurons are not like skin or blood cells that constantly replace themselves. They are meant to last a lifetime. That is exactly why the diseases in this section are so devastating. When these specialized cells die, the body usually cannot grow replacements, so the losses stack up and the damage is progressive and irreversible. Think of it like a city slowly losing its power lines one by one, with no crew coming to repair them.

Normally, healthy neurons keep themselves tidy. They fold their proteins correctly, clear out cellular garbage, and pass chemical messages (neurotransmitters) across tiny gaps called synapses. The neurodegenerative diseases each represent a different way this housekeeping and signaling breaks down, in a different neighborhood of the nervous system.

Alzheimer disease: the memory system clogs first

Alzheimer disease is the most common cause of dementia. The trouble is misfolded protein. Two abnormal proteins build up: beta-amyloid plaques collect in the spaces between neurons, and tau tangles (neurofibrillary tangles) twist up inside them. These deposits are toxic and jam the machinery that neurons use to talk and stay alive, so the cells wither and die. Because the damage often begins in the hippocampus, the brain's memory-forming hub, the first and loudest symptom is usually short-term memory loss, the person forgets recent conversations while old memories stay intact longer. As it spreads across the cortex, it steals language, judgment, and eventually the ability to recognize loved ones and perform basic self-care.

Parkinson disease: a dopamine shortage in the movement circuit

Parkinson disease targets a specific spot deep in the brain called the substantia nigra, a cluster of neurons that make dopamine. Dopamine is the chemical that smooths and starts your movements. As these neurons die off, dopamine drops, and the movement circuit (the basal ganglia) loses its balance. The classic picture is often summarized as TRAP:

• Tremor at rest, often a "pill-rolling" motion of the fingers that eases with purposeful movement
• Rigidity, stiff, cogwheel-like resistance in the limbs
• Akinesia/Bradykinesia, slowed and shrinking movements (small handwriting, a masked face, a shuffling gait)
• Postural instability, poor balance and a tendency to fall, usually a later sign

ALS: the motor neurons fail, but the mind stays sharp

Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig disease, attacks the motor neurons, the wiring that carries "move" commands from the brain and spinal cord to the muscles. Both upper and lower motor neurons degenerate, so patients develop progressive muscle weakness, atrophy, and fasciculations (muscle twitches), often starting in one hand or foot and spreading. The cruel twist is that in most patients cognition, senses, and awareness stay largely intact, the person remains fully alert inside a body that is losing its ability to move, swallow, and eventually breathe. Respiratory muscle failure is typically the life-limiting concern.

The common thread tying all three together is the one worth memorizing: a specific population of neurons is slowly and permanently lost, so symptoms only worsen over time. Current treatments slow progression or ease symptoms, they do not regrow the lost cells or cure the disease. That is why nursing care centers on safety, function, dignity, and family support. Explore the figure below to see where each disease strikes in the nervous system.

Section 6Demyelinating & neuromuscular disorders

Every time you lift a coffee cup, wiggle your toes, or take a breath, a tiny chemical conversation happens between a nerve and a muscle. That conversation takes place at the neuromuscular junction (NMJ), the specialized synapse where a motor nerve meets a muscle fiber. Understanding this handshake is the key to understanding why the disorders in this section cause weakness in such different patterns.

The neuromuscular junction: how the signal crosses

When an electrical impulse (an action potential) races down a motor neuron and reaches the nerve ending, it triggers the release of a neurotransmitter called acetylcholine (ACh). The ACh floats across the tiny gap (the synaptic cleft) and binds to nicotinic ACh receptors on the muscle membrane. That binding opens ion channels, the muscle membrane depolarizes, and the muscle contracts. An enzyme called acetylcholinesterase then chews up the ACh so the signal switches off cleanly and the muscle can relax. Three ingredients matter: enough ACh released, enough working receptors to catch it, and a healthy nerve to carry the impulse in the first place. Break any one link and you get weakness, but the pattern of that weakness tells you which link failed.

Multiple sclerosis: the insulation frays

Nerve fibers in the central nervous system are wrapped in myelin, a fatty insulation that lets impulses jump quickly from gap to gap. In multiple sclerosis (MS), the body's own immune cells attack and strip that myelin off CNS neurons (the brain, spinal cord, and optic nerves). This is autoimmune demyelination. Where myelin is lost, a plaque or sclerosis forms, and signals slow, scatter, or stop entirely. Because myelin can be damaged almost anywhere in the CNS, symptoms are famously scattered: blurred or double vision from optic neuritis, numbness and tingling, weakness, spasticity, fatigue, and bladder problems. The classic course is relapsing-remitting: flares appear, then partly fade as inflammation settles and some remyelination occurs, though scarring accumulates over time. A helpful teaching phrase is lesions separated in space and time.

Myasthenia gravis: the receptors get blocked

In myasthenia gravis (MG), the nerve and its ACh are fine, but the muscle's receptors are under attack. The immune system makes anti-ACh receptor antibodies that block and destroy nicotinic receptors at the NMJ. With fewer receptors to catch ACh, each signal lands weakly. The hallmark is fatigable weakness: muscles work at first but tire quickly with repeated use and recover with rest. This is why symptoms are typically worse at the end of the day. It classically strikes muscles that work constantly, causing ptosis (drooping eyelids), diplopia (double vision), and trouble chewing, swallowing, or holding the head up. The feared complication is myasthenic crisis, when respiratory muscles weaken and breathing fails.

Guillain-Barre syndrome: the nerves lose their coating from the outside in

In Guillain-Barre syndrome (GBS), the immune system attacks the myelin of peripheral nerves, often a week or two after an infection (frequently a GI or respiratory illness). This is molecular mimicry: antibodies aimed at the bug cross-react with nerve myelin. The signature is ascending paralysis, weakness and diminished reflexes that begin in the feet and climb upward, sometimes reaching the diaphragm and requiring ventilator support. Unlike MG, weakness is usually symmetric and progressive rather than fatigable, and it typically peaks then slowly recovers.

Explore the neuromuscular junction in the figure below to see where ACh crosses and where these diseases strike.

ReferenceWords worth knowing

A quick reference for the terms in this chapter — skim it now, or circle back whenever a word trips you up.

Bradykinesia

Slowness in starting and carrying out movement, a core motor sign of Parkinson disease that arises when degeneration of dopamine-producing neurons in the substantia nigra leaves the basal ganglia unable to smoothly initiate voluntary movement.

Cushing's triad

A late and ominous set of three vital-sign changes, hypertension with a widening pulse pressure, bradycardia, and irregular (often slow) respirations, signaling dangerously high intracranial pressure and impending brainstem herniation.

Demyelination

The loss or breakdown of the fatty myelin sheath that insulates axons, which slows or blocks nerve signal conduction and produces the neurologic deficits seen in diseases like multiple sclerosis.

Epidural hematoma

A collection of blood between the skull and the outer dura mater, usually from a torn middle meningeal artery after temporal trauma, classically causing a brief lucid interval before rapid deterioration.

Hemorrhagic stroke

A stroke caused by a ruptured blood vessel bleeding into or around the brain, which both deprives tissue of blood and raises intracranial pressure as the expanding blood compresses surrounding neurons.

Herniation

The life-threatening displacement of brain tissue across or through rigid intracranial structures (such as under the falx or through the tentorium or foramen magnum) when pressure builds, often compressing the brainstem and its vital centers.

Intracranial pressure

The pressure exerted inside the skull by the brain, blood, and cerebrospinal fluid together, normally about 5–15 mmHg, which becomes dangerous when a mass, bleed, or swelling pushes it higher.

Ischemic stroke

The most common type of stroke, caused by a clot or narrowing that blocks an artery and cuts off blood flow, starving a region of brain tissue of the oxygen and glucose it needs to survive.

Monro-Kellie doctrine

The principle that the skull is a fixed, rigid box, so an increase in any one of its three contents (brain, blood, or cerebrospinal fluid) must be offset by a decrease in another or intracranial pressure will rise.

Multiple sclerosis

A chronic autoimmune disease in which the body attacks central nervous system myelin, producing scattered plaques and a relapsing-remitting pattern of symptoms such as vision changes, weakness, and numbness.

Myasthenia gravis

An autoimmune disorder in which antibodies block or destroy acetylcholine receptors at the neuromuscular junction, causing fluctuating muscle weakness that worsens with use and improves with rest.

Penumbra

The ring of at-risk but still salvageable brain tissue surrounding the dead core of an ischemic stroke, which can be rescued if blood flow is restored quickly, which is why "time is brain."

Seizure

A sudden burst of abnormal, excessive electrical activity in the brain's neurons that can cause changes in movement, sensation, behavior, or consciousness.

Status epilepticus

A neurologic emergency defined as a seizure lasting 5 minutes or longer, or repeated seizures without full recovery in between, which risks permanent brain injury and requires immediate treatment.

Subdural hematoma

A collection of blood between the dura and the arachnoid, usually from torn bridging veins, which often bleeds slowly and may present days to weeks later, especially in older adults and those on anticoagulants.

tPA

Tissue plasminogen activator, a clot-dissolving (thrombolytic) drug given within a strict time window for ischemic stroke to break down the blocking clot and restore blood flow, but never used in hemorrhagic stroke.

DrillFlashcards for this unit

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