Chapter 19: Headache Assessment & Diagnosis
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Welcome back to the Deep Dive.
Today we are opening up the books, literally,
and tackling a subject that pretty much everyone listening has experienced.
But for a clinician, it can be an absolute minefield.
It really can.
We are digging deep into chapter 19.
Headache from the sixth edition of Advanced Health Assessment and Clinical Diagnosis in Primary Care.
It's good to be back.
And you're right, minefield is the perfect word for this.
Headache is, I mean, it's one of the most common complaints in all of medicine.
It's ubiquitous.
Right.
But as a primary care provider, your job is essentially finding a needle in a haystack.
Right, because the vast majority of headaches are just, well, they're just headaches.
They hurt, they're annoying, maybe they ruin your afternoon, but they aren't going to kill you.
Exactly.
The text lays it out very clearly right at the start.
One in 10 people will have a migraine.
That is a huge number.
And, you know, most headaches are acute, self -limited, and frankly, people handle them on their own with over -the -counter meds before they ever set foot in a clinic.
But, and this is the big but that finds this entire chapter.
Fewer than 1 % of headaches are caused by serious intracranial disease.
And that's our mission today, isn't it?
To decode that 1%.
We aren't just going to, you know, list symptoms.
We are going to walk through the logic of this chapter step by step.
Yes.
We need to understand how to distinguish the benign from the life -threatening using really nothing but history -taking, the physical exam, and solid clinical reasoning.
That is the goal.
We need to understand that 1 % without over -testing the 99%, and we're going to follow the chapter structure exactly.
So we'll start with the anatomy of what actually hurts inside your head, which is not what you think.
Right.
Then we'll move to the detective work of the history, then the hands -on physical exam, which is way more detailed than people realize, and finally, we'll break down the specific differential diagnoses.
So let's start at the very beginning.
The nature of the beast, as the book for students, or really anyone when they first start studying neurology, is the paradox of brain pain.
It is a massive paradox.
The brain tissue itself, the parenchyma, is not sensitive to pain.
At all.
Not at all.
You could hypothetically, and this happens during awake craniotomies,
you could poke the brain itself and the patient wouldn't feel it.
There are just no pain receptors in the brain matter.
Which is just wild to think about.
If the brain can't feel pain, why does my head feel like it's exploding during a bad headache?
What exactly is hurting?
It's the structures around and within the brain that are screaming at you.
The text is very specific about this.
We're talking about things like the venous sinuses, the dura mater, that tough outer covering of the brain.
The lining, basically.
Yeah, the lining, and the cranial blood vessels, and of course, all the extracranial stuff like your scalp, your facial muscles, and specific cranial nerves.
The text calls out the trigeminal, glosopharyngeal, and vagus nerves specifically.
Okay, so it's the plumbing and the wiring, not the computer itself.
That's a great way to put it, and the text points to figure 19 .1 here, which breaks down the actual mechanisms of pain.
It's not just one thing, is it?
It's not just pressure.
No.
No, and understanding this figure is crucial for understanding why different headaches feel so different.
It breaks it down into a few specific mechanical triggers.
Pain happens because of traction, literally pulling on those sensitive structures we just mentioned.
Pulling, like a tumor is stretching something.
Exactly, or it's inflammation, or it's vascular dilation when those blood vessels blow up like balloons,
or it can be simple muscle contraction, like an attention headache.
There's also a more complex one, dysregulation of the brain stem serotonergic systems.
That's a really big factor in how we understand migraines today.
It's a chemical thing.
So if something is pulling, swelling, stretching, or just chemically misfiring, you're going to feel it.
Now, moving through the anatomy section,
there's a specific landmark mentioned that seems crucial for localization,
the tentorium.
Can we break that down?
Because the text treats it like a road map.
Yes, the tentorium cerebellum.
It's essential.
Think of it as a tent or a rigid fold of dura mater that separates the cerebrum, the big top part of the brain, from the cerebellum, which sits below it.
It creates this physical divider inside the skull.
And this helps the clinician because it dictates where the patient actually feels the pain, right?
Exactly.
It provides a heuristic, a mental shortcut for localization.
So if the pathology, let's say a tumor or some swelling, is super tentorial, meaning above that line, right above the tent in the cerebrum area, the pain is generally felt in the front of the head, anterior.
And that's because that whole area is innervated by the trigeminal nerve, cranial nerve V.
Okay.
So front of the head, think top of the brain.
And if the problem is below the tent.
If it's infertentorial, so down in the cerebellum area or the brainstem, the pain is usually felt in the back of the head, posterior.
And that's because that area is innervated by different nerves, the upper cervical roots and vagus and glossopharyngeal nerves.
That is a super helpful mental model.
And obviously, if the problem is outside the skull entirely,
like a sinus infection, right?
If it's extracranial, like your sinuses or a tooth infection, the pain is usually felt right where the problem is.
There's much less referral of pain there.
It's more straightforward.
Okay, that makes sense.
So before we get into the real detective work of the history, we need to categorize these things.
The chapter makes a hard split, a really important one between primary and secondary headaches.
This is the first fork in the road for your diagnosis.
It's the first question you have to answer.
Primary headaches mean there is no structural or systemic pathology.
The headache is the condition.
The headache is the disease.
Correct.
And this accounts for more than 90 % of what you'll see in primary care.
And these are the famous ones, the ones we've all heard of.
The big four, essentially.
Migraine, tension type headache, or TTH, cluster headache.
And then there's a kind of catch -all category for other primary headaches.
Which leaves the secondary headaches.
And that's the scary category.
Right.
These are attributed to an underlying disorder.
This is where the headache is just a symptom of something else.
Trauma, a vascular disorder, like an aneurysm, an infection like meningitis,
substance withdrawal, or even a psychiatric disorder.
This is where the dangerous stuff usually hides.
And within that secondary category, the text then categorizes them by timing.
Acute, subacute, and chronic.
Why does that distinction matter so much?
Is it just for, you know, record keeping?
No, no.
It's not administrative at all.
It dictates your urgency and your differential diagnosis.
The clock tells a story.
An acute headache is a new onset.
That demands your closest attention because you don't know the trajectory yet.
It could be nothing or it could be a bleed.
And subacute.
What does that mean?
A subacute headache can be a warning sign.
It might be localized and precede deeper neurologic findings.
It suggests something is brewing, you know, but hasn't fully declared itself yet.
Maybe a slow growing tumor.
And chronic.
This seems like it would be less worrisome.
Generally, yes.
Chronic means it's been there a while.
But here is the critical point the text makes.
The major clue you're looking for in chronic headaches is a change in the usual pattern.
A change.
If a patient says, oh, I've had migraines for 10 years, that's one thing.
But if they say I've had migraines for 10 years, but this one feels different or the aura is different or they're happening every day now, that's a massive red flag.
Okay, let's unpack that change in pattern because that leads us perfectly into part two.
Diagnostic reasoning and the focused history.
The text says before you even ask about the pain, you have to check something else.
Orientation.
This is non -negotiable.
Before you ask, where does it hurt?
You need to assess if the patient is fully oriented to person, place, and time.
And the text specifically suggests using a quick tool like the mini cog.
The mini cog.
That's the three item recall and the clock drawing, right?
I always thought that was just for dementia screening in, you know, older adults.
It is often used there, but in context of a headache, it's a brilliant quick screen for cortical function.
It takes maybe 10 minutes, if that.
You ask them to remember three words, draw a clock face with the hands set to a specific time, and then recall the words.
It sounds simple.
But it's not.
It's not.
And if a patient with a headache has a mental status deficit on that screen, if they can't draw the clock correctly, for instance, you are essentially done with the interview history.
Done.
Like stop the appointment and send them home.
No, no.
Done in the sense that you are shifting into emergency mode.
Mental status changes plus headache equals immediate evaluation, and that likely means a CT scan right now.
You aren't going to sit there and ask about their diet triggers or if they ate chocolate yesterday if they can't draw a clock.
Because that implies the brain tissue itself is being affected.
Precisely.
It implies brain dysfunction, not just pain signals.
It's a whole different level of urgency.
Got it.
So that establishes the baseline safety.
So assuming they are oriented, they pass the mini cog, we get into the attributes of the pain itself.
The text highlights a few key questions.
Let's start with onset.
The scariest phrase in the headache world is sudden onset.
The thunderclap headache.
The thunderclap.
If a patient describes it as the worst headache of my life and it hit them instantly, I mean reaching peak intensity within seconds, like being hit with a baseball bat to the back of the head, that suggests a
hemorrhage.
And the text notes this is often precipitated by activity, right?
Like lifting something heavy.
Yes.
Often physical activity, straining, lifting heavy weights, coughing, even sexual activity.
It's an intense sudden onset.
And this is a surgical emergency until proven otherwise.
You have to be worried about a ruptured aneurysm leading into the space around the brain.
Okay.
That's the most dramatic onset.
What about trauma?
I feel like a trauma history can be really tricky because patients, especially older patients, might not even remember a minor pop.
It can be very tricky.
And the text does a great job distinguishing between the two big trauma outcomes you worry about.
Subdural hematoma and epidural hematoma.
You need to understand the mechanism, specifically the difference between veins and arteries, to catch these.
Let's break those down.
Subdural first.
Okay.
So subdural hematomas are common in older adults, often after They can also happen in alcoholics because of brain atrophy.
But here is the catch, the really sneaky part.
The symptoms can be delayed.
We're talking weeks, even up to a month later.
A month.
Why on earth does it take so long to show up?
Because it's venous bleeding.
Veins are low pressure.
So it's a slow leak and ooze.
It's not a dramatic gush.
So you might have an elderly patient who fell, seemed fine, went home, but weeks later starts getting confused or having headaches because that blood has been slowly slowly accumulating, pressing on the brain.
Versus the epidural hematoma, which is kind of the opposite mechanism.
Exactly the opposite.
Epidural is usually young adults, often associated with the skull fracture, particularly in the temporal area that tears the middle meningeal artery.
And arteries are high pressure.
Very high pressure.
So this happens fast.
This is a rapid bleed.
And this is the one with that famous lucid interval.
That's the one.
It's a classic tragic story.
The patient gets hit, maybe gets knocked out for a second, then wakes up and has a period of lucidity where they seem fine.
That's the lucid interval.
They might say, I'm okay.
Leave me alone.
But then they rapidly decline into a coma as that arterial pressure builds up a hematoma that compresses the brainstem.
It's dramatic and terrifying.
It is.
And it's why monitoring after any significant head trauma is so, so important.
So timing and trauma history are vital.
Let's talk about location.
We mentioned the tentorium earlier, but specific headache types have their own specific geographies described in the text.
They do.
And it's a very helpful clue.
Migraines are classically unilateral one side of the head, although it's important to know they can switch sides between attacks.
But during a single attack, it's usually on one side.
And tension headaches?
Almost always bilateral.
People describe a hat band squeezing the whole head or a heavy weight on top.
It's more diffuse.
And cluster headaches.
I hear those are very specific.
Incredibly specific.
Usually over one eye, orbital or periorbital.
It's often described as a hot poker being driven into the eye.
It is excruciatingly localized.
And what if it's a tumor?
Does a tumor hurt right where it is?
Tumors tend to cause pain in a discrete location that doesn't move.
And notably, the pain often changes with position.
So if the patient says leaning forward or coughing makes specific spot worse, that's a clue.
It suggests a mechanical shift or pressure change related to a mass.
Okay, that makes sense.
So besides the pain itself, we also have to look for associated symptoms.
These are the clues that kind of circle the headache.
Right.
You're looking for the company the headache keeps.
And this is huge.
For instance, if you have fever plus meningismus, that stiff neck where they can't lower their chin to their chest, you have to assume meningitis or encephalitis until proven otherwise.
That's a classic pairing.
What about visual changes?
Visual changes are a hallmark of migraines, specifically migraine with aura.
The text described this as a scintillating scotoma.
Which sounds beautiful, but I assume it isn't.
It is not.
It's twinkling lights, zigzag lines, or blind spots in the visual field.
It's a neurological phenomenon that precedes the pain.
If a patient sees that before the pain hits, it's a very strong indicator of migraine.
And nausea.
That seems common with a lot of headaches.
Nausea and vomiting are very common in migraine, absolutely.
But here is a specific red flag regarding vomiting that the text highlights.
Projectile vomiting.
Or, even more specifically,
vomiting without any nausea, especially in the early morning.
No nausea, just sudden vomiting.
That sounds bizarre.
It is, and it's very concerning.
That suggests increased intracranial pressure, or ICP, likely from a tumor.
It's a mechanical reflex, not a stomach bug.
The pressure in the skull is directly triggering the vomit center in the brain stem, so it bypasses that usual, I feel sick, nausea phase.
That is a crucial distinction.
The text also mentions vertigo.
Yes, and this is an interesting one.
About a third of migraine patients experience vertigo.
It can be part of the aura, or happen during the headache itself.
And this can sometimes lead to a misdiagnosis of an inner ear problem if you aren't careful to link it directly to the headache.
Okay, so we've got the symptoms.
Now we need to look at triggers and lifestyle.
This is where clinician turns into a bit of a lifestyle coach.
What are we looking for here?
Diet is huge.
Absolutely huge.
The text lists the classic tiramine -rich foods, things like aged cheese, red wine, chocolate is a big one, MSG, nitrates, and smoked meats like bacon or hot dogs.
The classic migraine triggers.
The classics, yes.
But then there's the environment.
And you must never forget carbon monoxide.
Never.
So CO poisoning.
Yes.
If a patient complains of headaches in the winter months when the furnaces are running, or if multiple family members have the same headache at the same time, you need to check the CO levels.
That's not a migraine, that's a poisoning.
That's a life -saving catch right there.
And medications, what about those?
Oral contraceptives are a big one, especially in the context of that stroke risk in migraineurs we'll get to later.
But also you have to look for the rebound headache,
medication overuse headache.
From taking too much Tylenol or Advil?
Exactly.
If someone is popping over -the -counter analgesics every single day, they might be causing the headache by withdrawing from the meds.
And caffeine withdrawal is another classic one, that weekend headache when you don't have your usual five cups of office coffee.
And finally, family history.
How important is that?
It's very important for differentiating the primaries.
The simple rule of thumb from the text is this.
Migraines have a strong genetic link.
If your mom had them, you're much more likely to have them.
Tension headaches.
Not really a genetic component.
So that's a good clue.
Okay, so that covers the history.
We've asked all our questions.
Now we actually have to touch the patient.
Part three.
The focused physical examination.
And this starts before you even touch them.
It starts with observation.
How is the patient acting in the room?
Okay, so if they're lying perfectly still in a dark room, curled up.
You're thinking migraine or meningitis?
Movement hurts.
They want the world to stop.
They are photophobic.
Afraid of light and phonophobic.
Afraid of sound.
But if they are pacing around the room, rocking back and forth, can't sit still.
That's classic cluster headache behavior.
The pain is so intense and piercing that they can't sit still.
They are agitated, holding their head, moving constantly.
They look like a caged animal.
The text also has a specific note here for pediatric patients.
Since a toddler can't tell you, I have a left -sided throbbing cane with photophobia.
What do we look for?
Right.
You look for the nonverbal cues.
Irritability is a big one.
Head rubbing.
And a very specific and very concerning sign called sunsetting eyes.
Sunsetting?
What is that?
It's where the eyes are driven downward, like the sun setting on the horizon so you can see the white sclera above the iris.
It's a sign of hydrocephalus increased fluid pressure in the skull.
It's literally pushing the eyes down.
It's a neurosurgical emergency.
Wow.
Okay, moving to vital signs.
We mentioned fever for infection.
What about blood pressure?
People always blame their headaches on high blood pressure.
They do, but it's usually not the cause.
The text is specific.
Severe hypertension can cause headaches, but usually only when the diastolic is greater than 130 mm Hg.
130 diastolic?
That's hypertensive crisis territory.
Exactly.
A mild elevation like 140 over 90 isn't typically the cause of the headache.
But you should keep an eye out for bradycardia, which is a slow heart rate combined with a narrow pulse pressure.
That can be a sign of increased intracranial pressure, part of what we call Cushing's Triad.
Okay, now let's get hands on.
Palpation.
We're actually palpating the skull.
You're feeling for tenderness?
If you tap on the skull and it hurts in one spot, that could be an abscess or local trauma.
But the most important thing you must do is palpate the temporal arteries.
This is on the side of the forehead in the temple area.
Yes.
You're checking for tenderness or a hard cord -like feeling.
That is a classic sign of temporal arteritis, also known as giant cell arteritis.
We'll discuss it more later, but it's an absolute emergency that affects older adults.
And you can listen to the skull, too.
Oscultation.
You can.
You can listen over the orbits or the skull for brutes, little whooshing sounds, which could indicate an AV malformation, which is a tangle of blood vessels inside the head.
The text also suggests checking the teeth, which seems a little odd.
It's not odd at all when you think about referred pain.
You tap the teeth with a tongue blade.
If it hurts, it might not be a brain tumor.
It might just be a dental root infection or maxillary sinusitis.
The nerves overlap and a toothache can easily present as a headache.
Right.
Okay, now the eye exam.
This feels like a critical part of the neuroassessment.
It is arguably the most important part of the physical exam for a headache.
You are looking for papildema, that swelling of the optic disc in the back of the eye.
Can you explain optic disc for those of us who haven't looked through an ophthalmoscope in a while?
Sure.
When you look into the eye with the scope, the optic disc is that circular area where the optic nerve enters the retina.
It should have crisp, sharper margins.
If the margins are blurry or the disc looks swollen and elevated, that is papildema.
It's a direct sign that the pressure inside the skull is high and is pushing forward against the back of the eye.
It's a window into the brain's pressure.
It is.
And then you have to check the pupils.
Right.
You're looking for anisocoria unequal pupils.
Exactly.
And if a patient has a headache and one pupil is blown dilated and fixed, meaning it doesn't shrink when you shine a light in it, that suggests an expanding lesion on that same side is compressing cranial nerve the third.
That is a very, very bad sign.
Speaking of cranial nerves, the chapter breaks down the assessment for almost all of them in the context of headache.
Let's just run through the big highlights.
CNI.
Olfactory.
Loss of smell could indicate a frontal lobe tumor compressing the olfactory nerve.
Optic nerve.
We just talked about papildema, but you're also checking visual acuity and visual fields.
A pituitary tumor, for example, often presses on the optic chiasm and causes something called bitemporal hemianopsia loss of peripheral vision on both sides.
A classic tunnel vision effect.
What about the eye movers, cranial nerves, third, four, and six?
Well, we mentioned CN third with the dilated pupil, but CN six, the abducens nerve is interesting.
Its job is to move the eye outward for lateral days because of its very long path inside the skull.
A CN deac palsy, a failure to look sideways, is often an early subtle sign of generalized intracranial pressure or hydrocephalus.
It's like the canary in the coal mine for pressure.
Wow.
CNV.
The trigeminal.
You test jaw strength and sensation on the face.
This is the nerve involved in trigeminal neuralgia, so you might find that just touching the face triggers that electric shock pain we talked about.
CN seven.
Facial nerve.
You're looking for asymmetry.
A hemiplegic migraine can actually mimic a stroke, causing facial drooping.
CN eight.
The acoustic nerve.
Unilateral deafness can be a sign of an acoustic neuroma, a benign tumor on that nerve.
And CN.
12.
Hypoglossal.
You have the patient stick out their tongue.
If it drifts to one side, it indicates weakness on that side, potentially from a stroke or a tumor affecting that nerve.
It's just amazing how much the face and the eyes can tell you about what's going on inside the brain.
Now we have to check the neck.
This is for meningitis primarily.
Correct.
You are testing for meningeal signs, starting with neutral rigidity.
You just ask the patient to touch their chin to their chest.
If they can't, or if it causes severe pain, that's a big red flag.
And the text lists two specific name signs.
Brzezinski and Kernig.
These are classic for your board exams, but they are also genuinely useful in the clinic.
Brzezinski's sign is when you, the examiner, flex the patient's neck forward and their hips and knees involuntarily flex.
They pull their legs up.
That's a positive sign.
And Kernigs.
Kernigs is when the patient is lying flat and you flex their hip to 90 degrees and then you try to straighten their knee.
If there's pain or resistance in the hamstring, that's a positive Kernig sign.
Both of these indicate meningeal irritation.
The lining of the spine and brain is inflamed and angry.
We also need to check coordination and gait.
This is all about testing the cerebellum.
You look for in a taxic gait.
That's a stumbling wide -based walk.
You ask them to tandem walk heel to toe, like on the sobriety test.
A positive Romberg test, where they fall over when they stand with feet together and eyes closed, suggests cerebellar or proprioceptive issues.
Before we leave the physical exam, I want to highlight this pediatric technique mentioned in the text.
I just love this one.
Draw your headache.
It's brilliant, isn't it?
Kids often lack the vocabulary to say photophobia or pulsatile or throbbing.
So you give them paper and crayons and say, show me what it feels like.
And what do they draw?
What does the text say?
If it's a migraine, they might draw flashing lights or zigzag lines or a picture of a dark room.
They might draw themselves lying down with a blanket over their head.
And if it's not a migraine?
For non -migraines, like tension headaches, they might draw pounding hammers on their head or a really tight band squeezing it.
It's actually a validated technique in the text, and it's surprisingly accurate for diagnosis in kids.
That is fascinating.
Okay, so we've done the history.
We've done the exam.
Now we have to confirm our suspicions.
Part four,
diagnostics and labs.
Right.
And the key here is we don't order imaging for everyone.
That's a huge point.
But when we do, we need to order the right test.
So CT scan versus MRI.
Who wins?
It depends on what you're looking for.
For a sudden, severe headache, especially if you suspect a hemorrhage or trauma CT is the first choice, fresh blood shows up bright white on a non -contrast CT.
It's fast, it's available, and it's great for bone.
And MRI.
MRI is much better for soft tissue.
If you suspect a tumor, an abscess, or an infection like encephalitis, MRI gives you the exquisite detail you need.
It sees the brain tissue itself much, much better than a CT can.
What about a skull radiograph,
an x -ray?
Does that have any role?
Very, very limited.
Really only for a post -traumatic bony assessment, like if you're checking for sinus fractures.
It won't tell you anything about the brain itself.
Now, labs.
There is one specific lab test mentioned as being critical for temporal arteritis.
The ESR, the erythrocyte sedimentation rate, or sed rate.
If you have an older patient with that tender temple we talked about, you order an ESR.
If it's elevated and the book says usually greater than 50 millimitridor, that strongly supports the diagnosis of temporal arteritis.
And the lumbar puncture, the LP.
This is the gold standard for meningitis, right?
It is.
You analyze the cerebrospinal fluid, the CSF, for cells, glucose, and protein.
But, and this is a massive safety warning in the chapter, it is absolutely contraindicated if you suspect high intracranial pressure.
Why?
What's the danger?
The danger is brain stem herniation.
If the pressure in the skull is very high from a tumor or swelling, and you release pressure from the spine below it by sticking a needle in, the high pressure in the skull can literally push the brain downward into the spinal canal.
And that's fatal.
That is fatal.
So, the rule is, you often get a CT scan before you do an LP to make sure there isn't a massive space -occupying lesion that could herniate.
And lastly, if you suspect the furnace is leaking, you order COHB levels.
Carboxyhemoglobin, a standard pulse oximeter won't catch carbon monoxide poisoning.
You need that specific blood test.
All right, we have all our data.
Now we have to put a name to the pain.
Part five, the differential diagnosis.
Let's start with the primary headaches, the most common one first.
Tension type headache, or TTH.
This is the stress headache everyone talks about.
It's bilateral, feels like a band.
It's non -throbbing.
It's annoying, but it usually doesn't stop you from going about your day.
And importantly, no focal neuroscience.
Okay, now contrast that with migraine.
Migraine is a whole different beast.
It's a neurological event.
It's usually unilateral.
It's throbbing or pulsatile.
And the pain is moderate to severe.
It's worsened by routine physical activity.
And it's accompanied by nausea, photophobia, light sensitivity, and phonophobia, sound sensitivity.
And the tech splits them into with aura and without aura.
Right.
Classic migraine is with aura, those visual changes, the scintillating scartoma we discussed.
Common migraine is without an aura.
There is a specific and pretty scary risk note here for women.
Yes.
And you need to know this.
Women under 45 who have migraines, particularly with aura, who also smoke,
and MD who use oral contraceptives, have a significantly increased risk of ischemic stroke.
That's a triad of risk factors you absolutely want to break up.
Good to know.
Next on the primary list is the cluster headache.
Cluster.
It's rare in children, much more common in men.
These are, by all accounts, some of the most painful conditions known to medicine.
They are abrupt, often waking people from sleep at night.
The pain is unilateral, orbital, and described as burning or piercing.
And they have those autonomic signs you mentioned, right?
Yes.
On the same side as the pain, you'll see eye tearing, a runny nose, maybe a constricted pupil, and eyelid drooping, which is called autosis.
And as we said, these patients pace.
They are agitated and can't stay still.
And the last primary mentioned is benign exertional.
Right.
This is a sudden splitting pain that happens right after exertion running, coughing, or sexual activity.
It's usually benign, as the name implies, but because the onset is so sudden, you often have to do a workup to rule out a subarachnoid hemorrhage first.
Okay, that covers the primaries.
Now let's move to the secondary headaches, starting with the infectious ones.
Sinusitis is a classic.
The pain is positional.
It's much worse when you bend forward.
You'll likely see purulent nasal discharge, maybe a fever,
and tapping on the maxillary or
the teeth hurts.
And meningitis.
The triad, fever, severe headache, stiff neck.
The patient looks toxic.
They look sick.
You might see patechial rash.
This is a medical emergency.
Get them to the hospital.
What about referred pain from dental or ear problems?
Very common.
An otitis media or a dental abscess can easily present as a headache.
You have to look in the ears and check the teeth.
Okay, let's move to the neurogenic or vascular secondary headaches.
We talked about temporal
Just to reiterate, because it's so important, age over 50, sharp temporal pain, a tender nodular artery.
The risk here is permanent blindness from occluding the retinal artery if it's not treated with high -dose steroids immediately.
And trigeminal neuralgia.
Those are the electric jabs or shocks along the nerve distribution on the face.
It's triggered by light touch, chewing, a cool breeze.
It's not a constant ache.
It's like lightning bolts of pain.
Optic anoritis.
This is pain with eye movement plus blurred vision.
It's often associated with multiple sclerosis or MS.
It can be the first presenting symptom.
Okay, secondary metabolic.
We covered CO poisoning.
What about hypoglycemia?
Low blood sugar can cause a generalized bilateral headache, but it usually comes with other symptoms like sweating, weakness, shakiness, and hunger.
Eating something should make it better.
Finally, the really scary ones.
Secondary structural and dangerous.
Intracranial tumor.
The pain here is progressive.
It gets worse over weeks or months.
And the key features are that it often wakes the patient from sleep, and it's typically worse in the morning.
Appieldema is often present on your eye exam.
That wakes from sleep detail is chilling.
It is.
A benign tension headache rarely wakes you up from a deep sleep.
A tumor, with its increasing pressure, very well might.
Subdural and epidural hematoma we covered.
Look for the trauma history and the mental status What about a brain abscess?
This will be localized pain.
You have to look for a history of a recent infection somewhere else.
A dental infection, an ear infection, or a sinus infection that could have migrated to the brain.
Or in kids, cyanotic heart disease is a risk factor.
And lastly,
pseudotumor cerebre.
Right.
Also known as idiopathic intracranial hypertension.
You see this usually in teens or menopausal women, often who are overweight.
It's associated with vitamin A overuse or tetracycline use.
They have all the signs of increased intracranial pressure, including papildema, but there's no tumor on the scan.
So we've reached the end of the chapter.
It's a lot of information.
It's pretty overwhelming.
It is.
But if we synthesize it, if we pull back, the clinician's role becomes very clear.
You are navigating from a completely subjective complaint, my head hurts, to an objective finding and a diagnosis.
The logical flow seems to be.
The history identifies the pattern.
The physical exam, especially the neuro and cranial nerve exam, identifies the localization and then diagnostics confirm the pathology.
That's it, exactly.
And the final thought I want to leave listeners with is about that delicate balance that the pecs describe so well.
Most headaches you see in your clinic will be tension or migraine.
They are benign.
But the outliers,
the temporal arteritis, the tumor, the subarachnoid hemorrhage, they don't always walk in with a neon sign over their head.
They present with those subtle clues you mentioned.
The morning vomit, the tender temple, the change in pattern, the worst headache of my life.
Your job as a clinician is to train your ears and your eyes to catch those whispers before they become screams.
Well said.
That's it for our deep dive into chapter 19.
Thank you for listening.
This has been the Last Minute Lecture Team signing off.
Good luck with your studies.
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