Headache (5) Flashcards
What are the three main types of primary headaches?
- Migraine
- Cluster headache
- Tension headache (both episodic and chronic types)
Difference b/n primary and secondary headache
Primary has no identifiable underlying cause whereas a secondary has an identifiable structural or metabolic cause
What characteristic way do subarachnoid hemorrhages present?
Sudden explosive onset of severe headache
*cerebral ischemia may also cause headache, can be seen in the post-ictal period following seizure as well
What are 9 causes of acute onset headache (get as many as you can, gay boy)?
- Subarachnoid hemmorhage
- Parenchymal brain hem.
- Subdural/epidural hem.
- Pituitary apoplexy
- Malignant HTN
- Acute closed angle glaucoma
- Carotid/ vertebral artery dissection
- Acute obstructive hydrocephalus
- Low pressure headache (CSF leak)
What are 8 causes of headache with subacute onset?
- Brain tumor/ other mass
- Meningitis/ encephalitis
- Cerebrovascular ischemia
- Cerebral venous sinus thrombosis
- Idiopathic intracranial HTN (aka Psuedotumor cerebri)
- Giant cell arteritis
- Chronic subdural hematoma
- Metabolic encephalopathies
What is responsible for the pain that causes headaches?
inflammation or physical traction of nerves fibers in structure in the head including meninges, vessels, scalp, and periosteum of the skull
*brain parenchyma itself has no pain fibers
What nerve innervates pain fibers from the supratentorial dura (nost of intracranial cavity)?
CN V
*Anterior fossa, middle fossa, and scalp
What nerves are responsible for the pain in the posterior fossa?
CN X (primarily); also CN IX and cervical nerve roots C2-3
What two places do pain fibers from the intracranial cavity synapse 1st beffore going to the VPL and VPM of the thalamus?
- Trigeminal nucleus caudalis
2. Dorsal horn of the upper cervical spine
What are 12 RED FLAG signs indicating a headache may be a possible secondary and therefore more dangerous etiology?
- Abrupt onset
- Hx of recent head trauma
- Fever
- Hx of immunosuppresion
- Altered conciousness
- Focal neurological symptoms/signs
- New onset in patient over 50
- Neck pain/ stiffness
- Anticoagulant use
- Headache progression over days
- Recently altered cognition
- “Worst headache of life”
What are three characteristics of migraine headaches in terms of presentation (including length)?
- frequently unilateral (may not always be on same side)
- pulsating
- Duration 4-72 hours
* relief usually seen after sleeping
* if always on same side, may merit a CT to look for an underlying cause
What are 3 associated symptoms frequently seen with migraine?
- Nausea (with or w/o vomiting)
- Photphobia and/or phonophobia
- May be preceded by a prodromal phase, including aura (in 20%)
Is there a genetic component to migraines?
Yes; 75% of patients have FHx of migraines
What are five symptoms that can be seen in a migraine prodrome?
- mood swings
- odd food cravings
- Malaise
- fatigue
- Muscle aches and stiffness
Other than visual aura, what are some other ways aura may present?
Can have transient limb weakness, sensory symptoms, transient aphasia—> therefore may mimic TIAs in some ways
*aura may also lead to fortification scotoma
What 3 main categories of triggers that may start migraines?
- Changes in daily cycles (no breakfast, menses, late hours)
- Environment or diet (weather, altitude, light, EtOH)
- Emotional (fear, anxiety, depression, anger)
At what age will most patients with migraines have presented?
age 20
may get better with age and many have decreased occurrence by 55
What sex are migraines more common in?
Females (only slightly—> 10-15% of woman, compared to 5-10% of men
*affects 15-25% of population, so fairly common
What nerve serves as the anatomical substrate for all migraines?
CN V–> CN V1 innervation of pain receptors in the dura, meninges, and medium/large cerebral arteries and veins that lie on surface of brain and above the tentorium
What anatomically is responsible for the vasodilation and other parasympathetic symptoms associated with migraines?
Central connections between pain pathways from CN V and the superior salivatory nucleus
*input from the trigeminal nucleus caudalis to the superior salivatory ganglion mediates parasympathetic signals to vessels via CN VII–>vasodilation
What two things initiate the nerve stimulation that leads to neurogenic inflammation of meningial vasculature responsible for pain in migraine?
- “Central Generator” (in patients that do not experience aura)
- Internal/external triggers in those with aura
*Either way, a wave of neural depolarization begins that excites already hypersensitized (via genetics or previous episodes) peripheral and central pain pathways
What is a cortical spreading depression? What does it do to blood flow initally, then right after?
A wave of brief neuronal excitation, which spreads across certain areas of cortex–> usually is followed by a period of prolonged depolarization (likely due to the sensitazion of the neuronal pathway)
*Blood flow is increased during the excitation, than oligemia (low blood flow) is associated with the phase in which there is prolonged depolarization
How is the scotoma and other transient losses in function associated with aura mediated?
The oligemia that accompanies the prolonged depolarization phase usually leads to a period of transient loss of function, regardless of where it occurs (makes sense, low blood flow = poor function)
*the deficit occuring during aura depends on where in the cortex the cortical spreading depression occurs
What part of cortex is responsible for visual disturbance in aura?
Cortical spreading depression in calcarine cortes of occipital lobe
What two chemicals are responsible for the pathogenesis of neurogenic inflammation/ pain in migraine?
- CGRP (especially)
- Substance P
*these can sensitize nerves to pain stimuli AND also directly cause vasodilation themselves–> vasodilation is the cause for much of th pain in migraine