headaches Flashcards
primary headache
these are headaches that occur independently and not caused by another medical condition
uncertain as to what sets the process of primary headaches into motion, involves blood vessels, intracranial and extracraial nerves, neurotransmitters, chemical mediators/pain modulators
most common primary headaches are tension headache, migraine headache, cluster headaches
migraine headache
Migraine with aura aka, classic or complicated migraine
Migraine without aura
Migraine without aura
Recurrent headache disorder manifesting in attacks lasting 4-72 hrs
Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and or photophobia and phonophobia
Diagnostic- at least 5 attacks, headache lasts 4-72 hr, headache has at least 2 of (unilateral location, pulsating quality, moderate or severe pain intensity, aggravation or causing avoidance of routing physical activity), during headache at least one (nausea and or vomiting, photophobia and phonophobia),
the migraine aura
comprised of focal neurologic phenomena that precede or accompany an attack- can be positive (gain of function) or negative (loss- of function) symptoms
Develop slowly over 5-20 minutes and last <60 minutes, usually visual, headache follows 80% of the time and usually begins within 60 mins
Migraine with aura (classic migrain or complicated migraine)
Important to get detailed aura history, Triptans, ergotamines and other vasoconstrictive meds should be avoided in migraine with brainstem aura and hemiplegic migraine
Persistent aura can occur–> migrainous infarct
Migraine with typical aura- typical aura with or without headache, with brainstem aura, hemiplegic migraine, retinal migraine
Migraine pathophys
- Peripheral trigeminal ganglion afferents innervate the meninges and large cerebral arteries
- Afferents from skin and muscles of neck converge on in the TCC together with afferents arriving from the meninges and cerebral vasculature
- Ascending connections from the TCC transmit signals to multiple brainstem, thalamic, hypothalamic, and basal ganglia nuclei
- Multiple cortical areas process inputs from TCC leading to phenotypic expression of migrain pain and symptoms
Activation of the trigeminal ganglion
Causes release of several vasoactive neuropeptides that are associated with neurogenic inflammation, Substance P, Neurokinin A, CGRP
Mechanisms of neurogenic inflammation and subsequent migraine pain: Vasodilation and extravasation of protein, increased platelet aggregation, activation of local immune response, mast cell degranulation
Cortical spreading depression–> migraine aura
Slowly propagating wave of depolarization/excitation followed by hyperpolarization/inhibition in cortical neurons and glia, Efflux of potassium, influx of sodium and calcium, release of glutamate ATP and hydrogen ions–> neuronal swelling break down of BBB: introduction of these proinflammatory molecules into meninges–> link between aura and headach
Non specific agents for migraine treatment
Acetaminophen, ASA, ibuprofen, Diclofenac, naproxen Na, indomethacin, combo (Acetominophen ASA and caffeine)
Antiemetics and prokinetics (given in adjunct to help nausea and vomiting, include (metoclopramide, prochlorperazine, ondansetron)
Specific Anti migraine drugs
Ergot derivatives Erg tart and dihydroergotamine)- agonist on 5HT receptors, has vasoconstrictor effects- Contraindicated in HTN, CAD, peripheral vascular disease, stroke, impaired kidney function and pregnancy
Interaction with many receptors–> more side effects (ergotamine>DHergo)
Intranasal DHergotamine migranal) most common in clinical practice and DHergotamine IV infusions for status migrainosus
Triptans- selective and highly effective 5HT receptor agonists, largely replaced the ergot derivatives, main mOA- intracranial extracerebral vasoconstriction, inhibition of NT release at peripheral and central trigeminal nociceptive terminals
Classes of preventative headache meds
Betablockers, Antiepileptics, antidepressants, BOTOX
tension type headache
Typically bilateral, pressing or tightening in quality, mild to moderate intensity, lasts minutes to days, does not worsen with routine activity, not associated with nausea or vomiting
10 episodes more than 1 day a month, 30 minutes-7days, bilateral location, pressing or tightening quality, mild or moderate intensity, not aggrevated by routine activity
Both nausea/ no more than one of photophobia/phonophobia
tension treatment
pharm- preventative (amitriptyline TCA, venlafaxine SNRI, Acute- simple and combined analgesics
Non pharm- relaxation, biofeedback, physical therapy
Avoidance of trigger factors- stress mental or physical, irregular or inappropriate meals, high intake of caffeine, dehydration, sleep disorders, reduced or inappropriate physical exercise, psychological problems
Cluster headache
Trigeminal
attacks of severe, strickly unilateral pain, often orbital, supraorbital, temporal, pain is associated with autonomic features
intensity can be excruciating (suicide headache)
Involves activation in the region of the posterior hypothalamic grey matter nocturnal attacks
cluster therapy
Acute therapy- given the excruciating pain, focus is on prompt relief, oral therapy is least effective, oxygen and parenteral triptans provide the fastest, most effective and reliable alleviation of pain
Short term preventative- corticosteroids are used as transitional therapy, includes IV methylprednisolone to break cluster period and oral prednisone, often added to long term preventative to help reduce the number and ntensity of cluster attacks in the begining of the episode compared to monotherapy with verapamil
Long term preventative- verapamil first line, lithium, topiramate, valproic acid
rigeminal neuralgia
characterized by recurrent unilateral brief electric shock like pains, abrupt onset and termination
May develop without apparent cause or may be result of another diagnosed disorder
Mild autonomic symptoms may present
following a painful paroxysm there is usually a refractory period during which pain cannot be triggered
Dignosis- recurrent paroxysms of unilateral facial pain in the distribution of one or more trigeminal nerve with no radiation beyond and fulfilling criteria B and C, Pain has all all of the following (lasting from a fraction of a second to 2 minutes, severe intensity, electric shock like shooting, stabbing or sharp in quality), precipitated by innocuous stimuli within the affected trigeminal distribution
trigeminal neuralgia treatment
focus is on prevention as attacks are short lived, first line Carbamazepine, others (gabapentin, topiramate, baclofen)
MR angiogram and CT angiogram may reveal vascular loop –> surgical decompression
secondary headache disorders
headache has developed in temporal relation to onset of causative disorder
Headache worsens in parallel with worsening of causative disorder
Headache has characteristics typical for the causative disorder
Other evidence exits of causation
What essential amino acid is serotonin synthesized from and the rate limiting step
Serotonin is made from tryptophan, the rate limiting step is tryptophan hydroxylase
Sythesis of 5HT
From essential amino acid tryptophan, tryptophan hydroxylase is the RLS, tryptophan concentration limits synthesis in the brain, (requires O2 and reduced pteridine cofactor), L aromatic amino acid decarboxylase is a similar enzyme used for catecholamine synthesis
The action of serotonin is terminated by and serotonin si converted to in the pineal gland
The action of serotonin is terminated by serotonin reuptake and monoamine oxidase and is converted to melotonin in the pineal gland
MAO metabolizes 5HT to 5hydroxyindole acetate, , neruonal action is terminated primarily by high affinity active uptake system (SERT) and then intraneuronal conversion to 5hydroxyindoleacetic acid
most of the serotonin in the body is in the gut and in the brain the serotonin neurons are promarily located in the raphe nuclei midbrain
Raphe nuclei isin the midbrain and brainstem
Project to hypothalamus, neostriatum, limbic forebrain, neocortex, medulla and sp cd, rapid turnover
serotonin receptors
At least 13 receptor subtypes, most are g protein coupled, there are neuronal autoreceptors, 5HT1 (inhibition of adenylate cyclase, 5HT1a also opens K channel)
5HT2- PI hydrolysis
5HT3- ligand gated cation channel
5HT4-7 activation of adenylate cyclase
Autoreceptors- decrease serotonin release 1 a and 1 d like
Serotonin in the CV and GI systems
CV- potent vasoconstriction of large arteries and veins, cranial blood vessels, vasodilation in coronary, skeletal muscle and cutaneous blood vessels, platelet aggregation active of serotonin from circulation
GI- synthesis and storage both neuronal and non neuronal - slow turnover 1day, contracts GI smooth muscle including esophagus, stomach and intestine- increasing tone perislasis and diarrhea, emesis- 5HT3 receptors in GIT and brain
CNS pharmacology
NT- Cell bodies in the midbrain raphe nuclei, project both rostrally and caudally,
Sensory perception, sleep slow wave deep sleep, temp regulation, neuroendocrine regulation- ACTH, GH, prolactin, TSH FSH and LH
Learning an memory esp short term
Pain, drug abuse, emestis - 5HT3 receptors,
Mental illness-
Affective disorders- SSRI and SNRIs
Schizophrenia- atypical antipsychotics
OCD SSRIs, Anxiety 5HT1a receptors, aggressive
