**_🧠Neurology🧠 - Headache Flashcards
How common are headaches?
One-year prevalence of headache disorders is 50%
20% of what neurologists see and care for
100,000 people absent from work or school every day
How can headaches be broadly subdivided?
Primary and secondary headaches?
What is the difference between a primary and secondary headaches?
Primary headache have no underlying cause, while secondary headaches are a result of other conditions (can be serious but serious causes are rare e.g. subdural haemorrhage)
What are the two subtypes of primary headache?
Long lasting (>4 hrs) and short lasting (<4 hours)
What headaches fall under the category of long-lasting headaches?
Migraines
Tension type headaches
(some medication overuse headaches, such as paracetamol)
What headaches fall under the category of short-lasting headaches?
Trigeminal autonomic cephalalgia (e.g. cluster headaches as the most common form)
What are the red flags for the clinical approach to headaches?
Secondary headache
Preliminary diagnosis of primary headache, however meets one of the SNOOP criteria - suggesting secondary headache
What is the SNOOP criteria?
Systemic
Neurologic
Onset (sudden)
Onset (age)
Pattern change
Papilledema
Pregnancy
Phenotype of rare headache
Elaborate on “systemic” as part of the SNOOP criteria
History of malignancy, immunosuppression, HIV, complaints of fever, chills, night sweats, myalgias, weight loss etc…
Abnormal systemic examination, incl. blood pressure and temperature
Elaborate on “neurologic” as part of the SNOOP criteria
Focal or global neurologic symptoms, such as changes in personality/behaviour, visual abnormalities, motor weakness, sensory loss etc…
Abnormal neurologic examination
Elaborate on “onset” as part of the SNOOP criteria
Onset, sudden - headache reaches peak intensity extremely quickly (<1 minute) - thunderclap headache
Onset, age - new-onset headache before age 5 or over age 65
Elaborate on “pattern change” as part of the SNOOP criteria
Progressive headache (changes in frequency to daily) or change in headache characteristics
Precipitated by the Valsalva manoeuvre
Postural aggravation
Elaborate on “papilledema” as part of the SNOOP criteria
The swelling of both optic discs in your eyes due to increased intracranial pressure (intracranial hypertension)
Elaborate on “pregnancy” as part of the SNOOP criteria
New-onset headache during pregnancy
Change in headache during pregnancy
Elaborate on “phenotype of rare headache” as part of the SNOOP criteria
Patient presents with symptoms consistent with that of trigeminal autonomic cephalalgia, hypnic, exercise-,cough-,or sex-induced
What is the pathophysiology of migraines?
(will not be examined, serves just for context)
Pathophysiology of Migraines
Triggering Factors:
Migraines can be triggered by various factors, including hormonal changes, stress, certain foods, and environmental changes. These triggers can lead to the activation of pain pathways in the brain.
Cortical Spreading Depression (CSD):
CSD is a phenomenon characterized by a wave of depolarization followed by a wave of hyperpolarization across the cortex.
This wave results in a transient disruption of neuronal activity, spreading over the surface of the brain.
CSD is believed to be responsible for the aura phase of migraines, causing visual disturbances or other sensory symptoms.
It also triggers the release of inflammatory mediators and neuropeptides, which contribute to the headache phase.
Activation of the Trigeminal System:
The trigeminal nerve (Cranial Nerve V) is involved in facial sensation and pain. During a migraine, it becomes activated, leading to the release of pro-inflammatory neuropeptides, including CGRP.
Trigeminal Ganglia: The cell bodies of trigeminal neurons reside in the trigeminal ganglia. During a migraine, these neurons become sensitized and facilitate the transmission of pain signals to the brain.
Sensitized trigeminal afferents lead to the release of inflammatory mediators, which promote vasodilation and further sensitization of pain pathways.
Role of Calcitonin Gene-Related Peptide (CGRP):
CGRP is a potent vasodilator and plays a key role in the pathophysiology of migraines. It is released from trigeminal neurons during a migraine attack.
Elevated levels of CGRP lead to increased vascular permeability and neurogenic inflammation, contributing to headache pain and associated symptoms.
CGRP antagonists (e.g., monoclonal antibodies targeting CGRP) have been developed as a treatment option for migraine prevention due to their ability to inhibit these pain pathways.
Neurogenic Inflammation:
The activation of the trigeminal system and the release of CGRP and other neuropeptides lead to neurogenic inflammation, characterized by vasodilation and increased vascular permeability in the meningeal tissues.
This inflammation contributes to the throbbing pain characteristic of migraines.
What is a visual aura?
Complex array of symptoms reflecting focal cortical or brainstem dysfunction
Gradual evolution: 5-20 minutes (<60minutes)
Usually before headache
What are some migraine preventatives?
(to be aware)
Outline the areas of the head felt by each headache type discussed in this deck
Summarise all three headache types
