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
