Headaches Flashcards
Primary vs secondary headaches
Primary Headaches: No obvious pathological cause, but a well-known syndrome of headaches, such as migraine, tension-type, cluster, etc.
Secondary Headache, or Headaches: A pathological cause can be found, such as tumor, hemorrhage, infection, etc.
PHYSICAL EXAMINATION
Concentrate on:
General appearance
Fever or other abnormal vital signs,
supple neck?
Mental status,
level of consciousness,
speech
Vision and the retinal discs: pupils, EOMI? Papilledema?
Asymmetry of strengths or reflexes in extremities,
Babinski sign
Secondary Headache Warning Signs and Signals
A single headache (versus recurrent headaches)
Sudden onset (thunderclap headache)
Onset of headaches after age 50 years
Recent onset of headaches, especially < 6 months
Systemic disease (malignancy, AIDS)
Change in headache pattern from a prior pattern
- Progressive headache with loss of headache-free periods
- Change in frequency or severity
Neurologic symptoms or abnormal neurologic exam
Lumbar Puncture
Necessary to diagnose meningitis or encephalitis, or possible carcinomatous meningitis
Can be used if there remains suspicion of subarachnoid hemorrhage but no blood is seen on a head CT or an MRI
When opening pressure is elevated, it can help diagnose pseudotumor cerebri, or Idiopathic Intracranial Hypertension,
Summary
Primary headache syndromes are diagnosed by defining the clinical features of an individual’s attacks and applying them to established definitions
The majority of headaches seen in primary care will be the primary headache disorders
If care is taken to identify warning signs and symptoms, and appropriate diagnostic tests are negative, the chance of missing a secondary headache is greatly diminished
Neuroimaging in Headache Patients
Recurrent migraine: neither CT nor MRI is warranted except
- Recent change in headache pattern
- Focal neurologic signs or symptoms
Nonmigraine headache: Role of CT or MRI is unclear
Role of CT versus MRI in headache patients is unclear, but MRI is more likely to show a cause for headaches;
CT is sensitive for > 90% of subarachnoid hemorrhages, and is faster than MRI
MRI without contrast might be indicated in pregnancy
Sometimes, You Can Feel It Coming: The Aura
Develops gradually right before attack and lasts less than an hour, often 20 minutes, in 10 – 15% of patients with migraine
Visual changes:
- Blurred vision or blind spots
- Seeing flashing lights
- Seeing jagged lines
- Difficulty in focusing
Sensory or motor changes:
- Numbness or tingling of the lips, face, or hands on one side of the body
- Weakness in arms or legs, usually on one side of the body
Speech or language changes:
- Inability to understand words
- Loss of speech or inability to speak normally
Aura symptoms frequently associated with migraine
Scotoma Teichopsia (bright, wavy lines)
fortification (zigzag patterns)
Photopsia (flashing lights)
Visual and auditory hallucinations
Paresthesias
Metamorphopsia (distorted size of objects)
MIGRAINE EPIDEMIOLOGY
It is true that nearly everyone gets an occasional tension type headache, but only a minority of patients with this type of headache seek medical attention for the headache
Migraine is the MOST COMMON HEADACHE THAT IS SEEN IN MEDICAL PRACTICE, since most migraine patients DO seek medical attention
About 15% of adult women and 6% of adult men have migraines in the United States, and 5 % of children
Migraines are more common in whites, less common in Africans, and least common in Asians
Professor Harold Wolff
After medical school and a neurology residency in the United States, Wolff dedicated his entire academic and clinical career to proving that there was indeed a pathology of migraine
He had migraine headaches himself
Determined to prove there must be a true pathological basis of migraines
Wolff: Where does headache originate?
- Not from the cerebral hemispheres; these neurons are completely insensitive, even to fire
Pain may come from:
- Arteries (Carotids, Middle Meningeal), and veins, including sinuses
- Meningeal distension or irritation of all 3 layers
- Periosteum of the skull, and inside the sinuses
- Cranial nerves V, IX
. Other scientists discovered: gray matter of pons is sensitive to pain
Wolff’s pathology of migraine
After decades of extremely invasive research on animals and many human volunteers, Wolff concluded:
- The aura of migraine results from a REDUCTION of blood flow to the occipital cortex in a visual aura, and the frontal or parietal cortices with other auras
- The actual pain of migraine results from an INCREASE in blood to the brain
- Wolff also discovered some kind of small molecule is secreted into the blood at the start of the headache
Migraine pathology
Released peptides can cause:
- Inflammation of the meninges and blood vessels, with cytokines and other inflammatory molecules
- Some vasodilation
Could Harold Wolff be wrong in his theory?
Yes, it looks like Wolff went too far! His ability to study decreases or increases in blood flow at that time was greatly limited by current technology
During a migraine aura, there is only a very slight reduction in blood flow
During the painful period of a migraine, the increased blood flow starts AFTER the pain begins
Blood flow during the aura
The reduction in blood flow to the cerebral cortex during an aura is a delayed, secondary event, due to these neurons lowering their electrical and metabolic activity
Essentially, there is a slow reduction in blood flow after the aura starts, which is a result of, not the cause of the aura
The actual reduction in perfusion is small
The neurogenic theory of migraine pathology,
as for the actual PAIN, of migraine, PET studies repeatedly show that regions of the pons, in the brainstem, become very active electrically up to 30 minutes BEFORE there is an increase in blood flow to the brain
At the beginning of the pain phase of migraine, the pons sends this increased frequency of depolarization and synaptic transmission to one or more adjacent trigeminal nerves, cranial nerve V
Migraine research disputes the vascular theory of migraine
THE NEURONAL THEORY OF MIGRAINE
Beginning in the 1980s, new technologies such as functional MRI and PET scans showed that there is only a trivial reduction in blood flow to the cerebral cortex during the AURA, and THIS CHANGE IN PERFUSION OCCURS AFTER a reduction of neuronal electrical activity This reduction in neuronal activity is probably the CORTICAL SPEADING DEPOLARIZATION that Leao had discovered many years before in animals with epilepsy
MIGRAINE PATHOLOGY
- This activation of the pons leads to increased activity in the trigeminal nerve which originates in the pons
- TRIGEMINOVASCULAR ACTIVATION is the name for this theory, as the cause of the actual pain of migraine
- The trigeminal nerve is both motor and sensory, with innervation of the face, arteries and veins, and meninges
- The trigeminal nerve releases multiple transmitters, including serotonin, Calcitonin Gene Related Peptide (CGRP), Substance P, and nitric oxide
Serotonin (5HT) and migraine
When large amounts of 5HT are released eventually its reuptake stops further release of this transmitter. Perhaps this is what ends the migraine attack.
Serotonin
As the migraine pain worsens, patients not only release serotonin from the pons and the trigeminal nerve, but from their own platelets
The enormous concentrations of platelet serotonin may go to these neurons and the meninges and blood vessels they innervate, and also help in preventing more transmitter release
5HT-1f RECEPTOR AGONISTS and migraine
Sumatriptan, and other triptans, are selective 5HT-1b and 5HT-1d and sometimes 5HT-1f RECEPTOR AGONISTS
They are very effective in ending the pain of migraine, but not the aura
Ironically, it was originally thought that serotonin agonists would stop migraine by reversing vasodilation
Migraine: Clinical Features
Nauseating “sick” headaches which are accompanied by light and often sound sensitivity, and are worse with activity
Build-up in intensity over @30 to 60 minutes
On average last one day, with a general range of 4 hours to 72 hours
About 15 – 20% of patients get an AURA of visual or sensory or motor deficits, for 20 or 30 minutes before the pain begins
Migraine Diagnostic Criteria
Migraine Criteria
>/= 5 attacks lasting 4–72 hours (30 minutes–7 days)
>/= 2 of the following
— Unilateral (bilateral)
— Pulsating (not pulsating)
— Moderate or severe intensity (mild or moderate) Aggravation by routine physical activity (not)
>/= 1 of the following
— Nausea and/or vomiting (no nausea/vomiting)
— Photophobia and phonophobia (one or neither)
No evidence on history or examination of disease that might cause headaches
migraine genetics
There must be a genetic component, since over 80% of patients have a close family member with migraines
Transmission is often mother to daughter
Genes have been found for Familial Hemiplegic Migraine, in which patients may have one sided weakness for days, along with the headache
Triggers of migraines
Environmental factors, often called “TRIGGERS,” are also important, since some patients get migraines only after head trauma
Many of the migraine patients have learned that certain foods can cause migraines, such as cheese, chocolate, diet drinks, red wine
Hormones matter, since about 75% of patients are women, and migraine often starts just after puberty, can end with menopause, and is very common during menstrual periods
More triggers and aggravating factors for migraines
Fasting- skipping meals/ eating specific foods/ caffeine intake
medication- analgesic overuse
Circadian Rhythms- changes in sleep/wake cycles
Environment- weather, - lighting, - fragrances/ odors
Hormones- PMS, oral contraceptives, pregnancy, menopause, menses
Stress/ Overexertion
Is migraine psychosomatic or pathological?
No pathology has ever been found in centuries of autopsies done on migraine patients
Migraine patients have much higher rates of psychiatric diseases than other people:
- Depression and bipolar disorder
- Anxiety disorders
- Personality disorders, especially borderline and narcissistic
Migraine center
dorsal raphe nucleus
Locus coeruleus
Tension Headache
Clinical Features
Dull, bilateral, squeezing, “tight,” nonpulsating pain
Routine physical activity does not aggravate pain
No vomiting and no more than one of
–Nausea
–Photophobia
–Phonophobia
Moderate or severe pain is less common
Musculoskeletal component, cervicogenic
Medication is seldom necessary for occasional tension type headaches
Tension type headaches
If these headaches are infrequent, and not too severe, few patients seek the help of their physicians
However, some patients may minimize their symptoms when they do describe their headaches, and they actually have migraines
Occasional use of over the counter analgesics is probably safe for tension type headaches
Chronic Tension-type Headaches
Average frequency > 15 days/month, with average duration > 4 hours/day if untreated and a history of > 6 months
History of less frequent headaches, when younger, is common
Gradual increase (evolution) over > 3 months
First of all, these patients must not take ANY analgesics more than once a week
Chronic tension type headache co-morbidities
- Co-morbidities…hypertension, depression, anxiety, insomnia, diabetes/hypoglycemia, other sources of pain, including the neck at levels C2 and C3
- Is there analgesic abuse, or prescription drugs for pain?
most common cause of daily headache
daily analgesics
Medication Overuse Headache
This is an enormous problem, in patients with BOTH migraine headaches and also tension type headaches, AFFECTING PERHAPS 2% OF ALL AMERICANS
Taking ANY PAIN PILL, either prescription or over the counter, from acetaminophen to narcotics, more than once per week causes INCREASED FREQUENCY OF HEADACHES TO EVERY DAY OR EVERY OTHER DAY
Formerly called REBOUND HEADACHE
The only true treatment is to limit or stop these drugs
Case Scenario :
36-year-old man
Has sudden, severe, stabbing
pain behind his right eye, spreading to the right temple
Headaches are
accompanied by
lacrimation and nasal
congestion
Pain 1 hour; attacks
occur daily for several
weeks, then stop for
months at a time
cluster headache
Cluster headache
The pain of a cluster headache is always in or close to one eye, the same eye, in every attack
The pain does not build up, it is IMMEDIATELY INTENSE
The pain may migraine a little toward the temple, but mostly stays around the orbit
So intense they are sometimes called SUICIDE HEADACHES
More common in men than women
Cluster Headache Autonomic features
conjunctival injection
lacrimation
congestion
rhinorrhea
swelling
miosis
ptosis
eyelid edema
Cluster Headache- epidemiology
Less common than migraines or tension type headache, perhaps 0.1% of people them
Brief, 15 min – 2 hour attacks, one-sided, in or around the eye; often 1 hour after falling asleep
Occur daily and/or multiple times a day for weeks or months at a time (season) and then disappear in most patients for a year or more
Intense pain which peaks rapidly, patients may walk about and even slam their heads into the wall
Pathology unknown: hypothalamic, and parasympathetic influences are possible
Some common secondary headaches
The pathology is not entirely known for these headaches or “facial pains,” but is thought to exist
It is important to consider these especially in patients who have abnormal vision or sensations, or systemic signs such as weight loss or fatigue
IDIOPATHIC INTRACRANIAL HYPERTENSION
ALSO CALLED: PSEUDOTUMOR CEREBRI
- Progressive diffuse headaches with intermittent loss of vision in one or both eyes, especially with eye movements
- Almost all patients are OBESE YOUNG WOMEN, rarely found in men; some association with estrogen and possibly progesterone supplements, Acutane for acne
- Increased intracranial pressure: due to overproduction of CSF? Brain swelling?
IDIOPATHIC INTRACANIAL HYPERTENSION- signs
Nearly all have papilledema, sen with the ophthalmoscope
Gradual, sometimes irreversible loss of visual acuity if not diagnosed early; patients may complain much more of a visual loss than headache when seeking medical help, so ophthalmologists often make the diagnosis
Often have an extraocular palsy
Diagnosis is supported by a significantly elevated opening pressure during lumbar puncture (well above 25 cm of water)
Idiopathic Intracranial Hypertension: treatment
The first or subsequent LPs may be therapeutic by removing some CSF
Successfully treated in most patients with WEIGHT LOSS, carbonic anhydrase inhibitors (which help synthesize CSF)
Severe cases may require surgery by an ophthalmologist (removal of the sheath around the optic nerves), or a shunt, removing cerebrospinal fluid continuously from the brain or the lumbar cistern
Trigeminal neuralgia, tic douloureux
A very brief, shooting pain lasting only seconds, or usually less than two minutes
Pain in one of the branches of CN V, usually maxillary or mandibular, rare in ophthalmic branch; many attacks per day, even in sleep
Pain is often “triggered” by touching the face, eating, shaving, brushing the teeth, applying lipstick or makeup; seldom occurs during sleep
Named by the French, as a repetitive spasm or “wince” of facial pain
Trigeminal neuraliga- who gets it, what to do
Most patients are over the age of 60, slightly more common in women
The majority of patients have no observable pathology, although there are numerous cases due to an enlarged artery or rarely, a tumor compressing the pons or the trigeminal nerve itself, or multiple sclerosis, a demyelinating disease
Consider a brain MRI in patients, especially if they have other symptoms and signs
Giant Cell Arteritis
Also known as Temporal arteritis
An example of vasculitis, or a non-infectious inflammation of arteries, leading to gradual occlusion at some locations
Involves the superficial temporal artery, a branch of the external carotid artery, on one and rarely both sides
May spread to the adjacent internal carotid artery, reaching the ophthalmic artery and causing COMPLETE VISUAL LOSS via ischemia
Giant Cell Arteritis- who gets it
Almost unheard of in patients under the age of 50, so a concern for elderly patients getting their first headaches
Accompanied by fatigue, difficulty chewing, and pain in the neck and shoulders
Probably part of the spectrum of Polymyalgia Rheumatica
Diagnosis suggested by elevated Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein, and confirmed by superficial temporary artery biopsy
Giant Cell Arteritis- diagnosis, what to do
Curable if the patient is given prednisone within the first weeks of the onset, typically 60mg per day or more, gradually and slowly decreased over many months
It is crucial to diagnose this disease before there is any visual loss, which may be permanent
If the diagnosis is strongly suggested, begin prednisone immediately, or right after confirmatory blood tests and, before a biopsy can be scheduled
