10.13 Headaches Flashcards
Classify headaches
Primary (disorder of nervous system)
- migrane
- tension-type headache
- trigeminal autonomic cephalalgias
- cluster headache
- other
Secondary (manifestation of other disorder)
Neuropathies, facial pain and other headaches
Tension type headache
Epidemiology + General
Signs & symptoms
- most common head ache disorder
- High prevalence
- Females
- Precipitants: Stress and mental tension
- Migraine and TTH = related conditions with shared environmental and lifestyle factors
- Migraine may precipitate or aggravate TTH
Signs & Symptoms
- Muscle tenderness in the head, neck, or shoulders is associated with both the intensity and the frequency of TTH attacks
- Pericranial muscle tenderness can be elicited from the history or confirmed on examination by manual palpation
Pathophysiology of tension-type headache
Nociceptor sensitization
- Peripheral activation of myofascial nociceptors
- Sensitization of central pain pathways
- ⬆️facilitation & ⬇️ inhibition of pain transmission
Peripheral factors
- Increased muscle tenderness
- Origin of muscle tenderness is unknown, nociceptors around blood vessels in striated muscle, tendon insertions, and fascia have been suggested as sources of the pain
Genetic factors
- Hereditary factors play a minor role
Migrane
- complex disorder of which the most debilitating symptom is severe headache
- female (adult)
- in childern = male
- family history
- without aura = most common
- initial attack in adolescence
- tends to recur with varying frequency throughout life, and attacks tend to get milder and less frequent in later years, although this certainly is not a universal finding
- some pt may experience symptoms of transient neurological dysfunction called “aura” along with their headache – “classic” migraine
Features of migrane
- Headache= typically episodic, unilateral, throbbing head pain of moderate to severe intensity
- Many patients, however, describe the pain as steady while they remain still
- head throbs with pulse in head- low position
- pain tends to worsen with routine physical exertion and jolts
- pain builds up over 30 min (crescendo), rarely explosive
- if untreated, persists from 4 hours up to 3 days
- improvement occurs gradually (decrescendo)
- there are specific identifiable triggers
Terminology of migraines
- Classic migraine: migraine with aura
- Common migraine: migraine without aura
- Menstrual/catamenial migraine
- Status migrainosus: an attack that lasts more than 72h
- Retinal migraine (visual migraine)
- Migraine equivalent: aura without headache
- Premonitory phase (warning that migraine may start)
- Postdrome (migraine hangover)
Autonomic dysfunction in migranes
- lightheadedness
- facial oedema
- pre syncope/ syncope
Pathophysiology of migraine
- Primary neuronal dysfunction lead to the manifestations
- Cortical spreading depression is a self-propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex
- Cortical spreading depression is hypothesized to
➡️Cause the aura of migraine
➡️Activate trigeminal nerve afferents
➡️Alter blood-brain barrier permeability by matrix metalloproteinase activation and upregulation - The activation of trigeminal afferents by CSD in turn causes
inflammatory changes in the pain-sensitive meninges that generate the headache of migraine through central and peripheral reflex mechanisms
Migraine aura
- focal cerebral symptoms associated with a migraine attack
- consists of transitory visual, sensory, or language disturbance or other focal cerebral or brainstem symptoms (“basilar migraine)
- Symptoms typically last 20-30 minutes but can last 1 hour and usually precede headache
- May continue into the headache phase or begin during the headache
- Aura occurs in about 20% to 25% of migraineurs and generally does not occur in every attack
- visual aura spreads across the visual field slowly, taking as long as 20 minutes to reach maximum, the paresthesias may take 10 to 20 minutes to spread from the point at which they are first felt to reach their maximal distribution
- slower than the spread or march of a sensory seizure and much slower than the spread of sensory symptoms of a TIA
- A migrainous sensory aura generally resolves over the course of 20 to 60 minutes
Visual aura
Visual symptoms are most common
- Consist of either positive (flickering lights, spots, or lines) or negative (scotomas or visual field loss) phenomena or both
- Characteristically affect both eyes
Basilar-type migraine
Epidemiology
Evolvement of migraine
- Manifestation of an immature CNS
- children and adolescents
Evolvement of migraine:
- Typical aura (10-45min) preceding occipital headache
1. *visual aura:** teichopsia, greying of vision, bilateral blindness
2. sensory aura: paraesthesiae of lips, hands and feet
3. brainstem signs: ataxia of gait and speech, vertigo, diplopia, tinnitus, dysarthria
4. depressed LOC from which pt is transiently rousable, due to RAS involvement, as other aura subside
5. occipital headache which may become holocephalic, with vomiting, resolving after sleep
Trigeminal autonomic cephalalgias (TACS)
Define
Symptoms of pain
Def - A distinct set of headache disorders typified by:
- Shorter-lasting attacks of unilateral intense pain in the trigeminal distribution (typically V1)
- Along with ipsilateral cranial autonomic symptoms
Symptoms (In contrast to migraine, the pain is:)
- Almost universally unilateral
- Prominently located in the V1 distribution
- Shorter-lasting (with the exception of hemicrania continua), and
- More intense
Pathophysiology of TACS
- trigeminovascular system is the pain component of TACs
- V1 branch of the trigeminal nerve, which receives inputs from the forehead, eye, dura, and large cranial vessel
- Projects to several nociceptive nuclei in the brainstem and upper cervical cord (trigeminocervical complex, which includes the occipital nerve)
- Projects to the thalamus, and finally to the pain neuromatrix (a collection of brain areas that modulate many types of pain)
- Autonomic system = lacrimation, conjunctival injection, and other cranial autonomic features (parasympathetic overactivation or sympathetic inactivation)
- Hypothalamus= circadian system and aggression areas (explains clocklike regularity of cluster headache and the restlessness seen in patients with TACs)
Cluster headache
Core features
Pain features
Core features
- Circadian periodicity in terms of active and inactive periods over time
- Lateralization of the pain and autonomic and related symptoms
- Agitation during attack (anxiety)
Pain features:
- abrupt onset
- onset preceded by brief sensation of pressure in soon-to-be-painful area
- typical location of pain is retro-orbital and temporal regions (upper syndrome) but may be maximal in the cheek or jaw (lower syndrome)
- pain feels steady or boring and of terrible intensity (“suicide headache”)
- Intensifies very rapidly, peaking in 5-10 min and usually persisting for 45min to 2 hours
- occur at night and lead to sleep deprivation
- Toward the end of the attack, brief periods of relief may be followed by several transient peaks of pain before the attack subsides over a few minutes
Paroxysmal hemicrania NB!
Epidemiology
Signs and symptoms
Epidemiology
- Typical onset in the third decade of life
- Female-to-male ratio is approximately 1:1
- Chronic form more common (65%)
Signs and symptoms
- Episodic form characterised by daily attacks for active period (4-24 weeks), followed by a remission period (12-376 weeks)
- Attacks characterised by sharp, stabbing or throbs of pain (V1 > C2)
- Each paroxysm accompanied by at least one robust ipsilateral autonomic feature
Post-concussion syndrome (PCS)
General
Epidemiology
Symptoms
- Headache = most common physical symptom following traumatic brain injury, may not occur in isolation
- may be part of a symptom complex known as post- concussion syndrome which comprises physical, psychological and cognitive symptoms
- Loss of consciousness does not have to occur for PCS to develop
Epidemiology
- female
- increasing age
- 30-80% of patients with mild traumatic brain injury (TBI) will experience some symptoms of PCS
Symptoms
- fatigue
- headache
- dizziness
- memory trouble
- trouble sleeping
- trouble concentrating
- irritability
- blurred vision
- anxiety
- increased light and sound sensitivity
- More severe injuries tended to be associated with a greater proportion of cognitive and psychological symptoms in addition to physical symptoms
Giant cell Arteritis
A systemic inflammatory vasculitis that occurs exclusively in older adults
• Peak incidence in the seventh decade, highly unlikely in those <50 years
• It causes idiopathic granulomatous inflammation of the large- and medium- sized arteries
• May produce a wide spectrum of clinical manifestations depending on the predominant pattern of involvement
The headache is due to inflammation of the cranial arteries, especially branches of the external carotid artery
• Headache quality and systemic symptoms are variable!
• Systemic symptoms: polymyalgia rheumatica, jaw claudication, raised ESR
• Neurological manifestations
• Amaurosis fugax, persistent visual loss due to anterior ischemic optic neuropathy (AION), stroke, dementia
• AION is an emergency!
• Time interval between visual loss in one eye and in the other is usually less than 1 week, and can be prevented by treatment
• Temporal artery biopsy confirms the diagnosis
Vascular dissection
Separation of the arterial wall layers results in dissection - a false lumen arises in the space where blood seeps into the vessel wall, and occludes the true lumen
• These are generally caused by various degrees of trauma or triggering events, including
• Childbirth
• Cervical manipulation therapy • Coughing or sneezing
• Minor sports injuries
• Roller coaster rides
• Vigorous exercise
Local symptoms caused by cervical or cerebral artery dissection can include
• Head and neck pain
• Horner syndrome
• Cranial neuropathies, e.g. XII, then IX
• Pulsatile tinnitus
• Ischemic stroke or transient ischemic attack
Low versus high pressure headaches
Idiopathic intracranial hypertension
• Papilloedema
• Pulsatile tinnitus
• Transient visual obscurations
• Sixth nerve palsy
The headache quality is not typical of the raised ICP headache
Intracranial hypotension
• Headache improves on lying down and Trendelenburg
• Headache worsens as the day progresses
• No papilloedema – venous pulsations are often observed
• Nonpulsatile tinnitus
Both may have sixth nerve palsies, and worsen with Valsava, exercise or bending over
Trigeminal neuralgia
Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C
A.
Pain has all of the following characteristics:
1. lasting from a fraction of a second to 2 minutes
2. severe intensity
3. electric shock-like, shooting, stabbing or sharp in quality
Precipitated by innocuous stimuli within the affected trigeminal distribution
Not better accounted for by another ICHD-3 diagnosis
Most cases are caused by compression of the trigeminal nerve root, usually within a few millimeters of entry into the pons (the root entry zone)
• Compression by an aberrant loop of an artery or vein is thought to account for 80 to 90% of cases
• Other causes include vestibular schwannoma, meningioma, epidermoid or other cyst
• Compression of the nerve may lead to focal demyelination with ectopic impulse generation that may stimulate neighbouring fibers (ephaptic transmission)
Other than the triggering phenomenon, most patients with TN fail to show sensory abnormalities within the trigeminal distribution
• If clinical neurological examination show sensory deficits, this should prompt imaging investigations
• When very severe, the pain often evokes contraction of the muscles of the face on the affected side (tic douloureux)
• Mild autonomic symptoms such as lacrimation and/or redness of the ipsilateral eye may be present
Episodic cluster vs Chronic cluster
Episodic cluster(90%)
- Cluster period: 7 days to one year
- Cluster period is consistent for a given patient
- Pain-free periods: one month or longer
- Common pattern is two cluster periods per year
- With time, clusters may become seasonal, then occur more often and last longer
Chronic cluster(10%)
- Attacks of pain occur for more than 1 year without remission or with remissions lasting less than 1 month
- May develop de novo or may evolve from episodic cluster headache
