10 free Paramedic practice questions: Advanced Neurologic Emergencies

Give an antihypertensive for the bleed: A systolic of 222 pushes people toward a bleed, and lowering pressure in a bleed is a real hospital treatment. You cannot tell which stroke this is without imaging, and in an ischemic stroke that pressure is what perfuses the tissue around the clot. The hospital sets pressure targets once it knows what it is looking at.

Hyperventilate to lower intracranial pressure: Hyperventilation does drop carbon dioxide and constrict cerebral vessels, so it sounds like a way to buy room inside the skull. That constriction starves a brain already short of flow, and it is reserved as a brief bridge for active signs of herniation. Nothing here shows herniation, so ventilate to normocapnia.

Position the patient flat for perfusion: Lying a patient flat raises pressure inside the head by slowing venous drainage out of it, which is the opposite of what this brain needs. Students borrow the position from shock care, where raising perfusion is the goal. Elevate about 30 degrees and keep the neck midline.

A vagal response to the vomiting: Vomiting really can drop a heart rate through a vagal response, and the patient did vomit, which makes this feel like it explains the 44. A vagal episode does not come with a systolic of 198 and irregular respirations. It also does not make one pupil dilate.

Decompensated shock from the bleed: A bleeding brain suggests blood loss, and students carry shock into any hemorrhage. Decompensated shock is hypotension with a fast, weak pulse, and this patient is hypertensive and bradycardic. Intracranial bleeding kills through pressure inside a closed skull, not through volume lost.

An opioid effect on the brainstem: Respirations of 8 in an unresponsive patient is the pattern that makes everyone think of opioids, and it is worth ruling out on many calls. Opioid effect brings small, equal pupils, and this patient has a 6 mm pupil on one side. The sudden severe headache before the collapse points somewhere else.

Midazolam: A benzodiazepine is first-line for almost every seizure you will meet, and that habit is strong. Eclampsia is the named exception to the algorithm. Magnesium sulfate is what treats the eclamptic process itself, while a benzodiazepine can quiet the convulsion without touching what is driving it, which is why magnesium is the drug here.

Levetiracetam: a genuine second-line agent for a seizure that has not responded to two benzodiazepines. Nothing has been given yet, so there is no failed first-line drug to escalate from. Second-line agents also do not address what is driving an eclamptic seizure.

Dextrose: Checking a blood glucose level on every seizure is correct, and it is the fastest reversible cause to find. This blood glucose level is 98 mg/dL, so there is nothing to correct. Giving dextrose to a patient with a normal glucose treats nothing and delays the drug that would work.

Thiamine deficiency producing an encephalopathy: Chronic heavy drinkers really are thiamine depleted, and that deficiency causes a brain problem worth treating. It shows up as confusion, eye movement changes, and an unsteady walk rather than as a single generalized seizure at the 30 hour mark.

A first presentation of an ordinary seizure disorder: A first seizure in an adult does deserve a workup, and sometimes that is what it turns out to be. A new disorder does not explain why this seizure arrived on the second day without alcohol, and settling for it lets the crew miss what comes next.

Acute alcohol intoxication lowering the seizure threshold: Alcohol and seizures do travel together, so blaming the drinking is a reasonable first thought. Alcohol is a depressant while it is on board and the seizure risk arrives on the way down, which is why the time since the last drink is the fact that matters.

It is incidental here, since only a low glucose harms the brain: Almost everything you were taught about checking a glucose is aimed at catching a low one, and in a stroke that is the mimic that matters most, so reading a high number as background noise has real logic behind it. A high glucose is its own insult to tissue that is already starving for flow, which is why the target is a normal sugar rather than simply a sugar above the floor.

It explains the weakness, so treat the high glucose as the problem: Diabetes sitting next to an altered patient is a pairing that gets treated as a sugar problem every day of the week, and the history is right there in front of you. A level of 268 does not produce one-sided weakness or slurred speech, and a patient with warm dry skin, a pulse of 78, and quiet breathing is not in a hyperglycemic crisis.

It calls for a fluid bolus to bring the glucose down before arrival: Fluid is the backbone of care in the hyperglycemic emergencies, so reaching for a bolus when the number is high is a habit built on real practice. This patient has no volume deficit to replace and a bolus does not meaningfully move a glucose level, so it spends effort on the one number you cannot change in the field.

A complete cord transection: A deficit this striking can read as a cord cut through, and the mechanism here really is a blade. A complete injury leaves nothing below the level on either side, and this patient still moves the right leg and still feels pinprick on the left, which makes the injury incomplete.

Anterior cord syndrome: Anterior cord also produces a dramatic motor deficit, which puts it on the list for any cord injury. Its pattern is not sided, since motor function goes along with pain and temperature while position sense, vibration, and light touch survive. This patient lost position sense on one side and pain on the other.

Central cord syndrome: Central cord is the incomplete syndrome most people name first, because it is the one they see. It runs arms worse than legs after a hyperextension injury, classically in an older patient with a narrowed spinal canal, and nothing about one stab wound in a 24-year-old matches that.

A subdural bleed, because venous blood collects over hours: Subdural bleeds are common and they belong on the list for any head strike. Venous pressure fills a space slowly, so subdurals take hours to days to declare themselves rather than 25 minutes.

A diffuse axonal injury, because shearing deficits appear early: Shearing injury is worth considering after any violent head movement, and it does produce a profound deficit. Its deficit is present from the moment of injury rather than arriving after a stretch of normal conversation.

A subarachnoid bleed, because it is at its worst from the start: A sudden severe presentation does fit a subarachnoid bleed, and those patients do decline. That bleed is at its worst the instant it starts, which is the opposite of the quiet interval this patient had.

An epidural bleed from a torn middle meningeal artery: An epidural bleed is the classic rapid decline after a head injury, so reaching for it is natural. It comes from a blow to the side of the head that usually leaves a mark, and it produces a lucid interval rather than a deficit present from the first moment.

A basilar skull fracture with bleeding into the sinuses: Basilar fractures come from serious mechanisms like this one, so the thought fits the crash. A basilar fracture announces itself with bruising around the eyes or behind the ears and fluid from the nose or ears, and none of that is present.

A depressed skull fracture pressing on the motor cortex: A depressed fracture does press on brain tissue and it can cause a focal deficit. You can usually see or feel the depression, and this head has no wound, no swelling, and no deformity anywhere.

Hyperventilate through the attempt to hold the pressure down: Hyperventilation does lower the pressure inside the skull, and it has a narrow role when a patient is actively herniating. Routine hyperventilation constricts cerebral vessels and cuts flow to tissue that is already starving, and this patient has no herniation signs to justify it.

Use a full induction dose so the first attempt is not interrupted: A deeper patient is an easier patient to intubate, and a failed first attempt costs time you do not have. A full induction dose at 86 systolic buys that first pass with a hypotensive episode, and one of those roughly doubles mortality in a severe head injury.

Skip preoxygenation to shorten the time without ventilation: Shortening the apneic time sounds protective, and speed does matter when a patient is desaturating. Preoxygenation is what buys the safe seconds during the attempt, and skipping it at 87 percent guarantees the hypoxic episode you were trying to avoid.

Remove the collar and hold manual stabilization instead: Manual stabilization is a legitimate technique and it does avoid the pressure a collar puts on the neck. Holding a head by hand for an entire transport is not practical, and it does not fix the real problem, which is a strap position and a head that is not midline.

Tighten the straps further and pad under the head: Secure packaging is drilled into everyone, and a patient who shifts during transport is a real problem. Tightening a strap across the sides of the neck squeezes exactly the veins the head drains through, so the security comes at the cost of the pressure inside the skull.

Leave the packaging as it is and raise the foot end: Raising the foot end is the reflex for a patient with a pressure problem, and it does move blood toward the core. Putting a head injured patient head down raises the pressure inside the skull, which is the opposite of what this patient needs.