Headache and Dizziness/Vertigo Surat Tanprawate, Tanprawate, MD, MSc(Lond.), FRCPT Division of Neurology Chaing Mai University
The Northern Neuroscience Centre Chiang Mai University
NNC CMU
Worldwide prevalence of headache
Rigmor Jensen, The Lancet (2008) (2008)
The Northern Neuroscience Centre Chiang Mai University
NNC CMU
Lifetime Prevalence of Headache Type
Prevalence (%)
Primary headache TTH Migraine
78 16
Secondary headache Fasting Nose/sinus disease Head trauma Non-vascular intracranial disease (including brain tumor)
19 15 4 0.5
Pain
René Descartes, French Philosopher 31 March 1596 – 11 February 1650
Understanding pain sensitive structure in the head Harold Wolff and Bronson Ray(1940) • Observe that the mechanical stimulation of the brain parenchyma did not cause pain in awake patients who were undergoing craniotomies but that similar stimulation of the meninges and cerebral and meningeal blood vessels produced severe, penetrating, ipsilateral headache
Ray, B.S. and H.G. Wolff. Wolff. (1940). Experimental studies on headache. Pain-sensitive structures of the head and their significance in headache. Arch. Surg. 41:813 - 856.
Ray and Wolff method • Surgical exposure of structures within and outside the cranium • The observation were recorded (localization, what kind of stimulation) in operating room • 30 patients with local anesthesia: • extra- and intracranial structure • : Scalp, galea, fascia, muscles, arteries, vein, sinuses
Scalp, galea (epicranial aponeurosis), fascia, muscles: --150 observations, 30 subjects --thermal,chemical, mechanical, electrical stimulation
Ventricles, Ventricles, aqueduct of Sylvius, Choroid plexuses --24 observations, 4 subjects --a balloon placed through a small opening into anterior horn and body of lateral ventricle
Dural artery (middle meningeal artery): --96 observations, 11 subjects --stimuli: faradizing, distending, stroking,
Ray and Wolff(1940)
Headache and Pain Sensitive Structure Meninges Venous sinus Artery: Artery: -dural a. -carotid a. -basilar a. Neural structure: structure: -glossopharyngeal n. -trigeminal n. -upper cervical n.
!"#$%%&'()*+,-.+/0*#
International Classification of Headache Disorder (ICHD-3 Beta) Part 1. 1. The primary headaches - Migraine, TTH, CH and other TACs, and other primary headache disorder Part II. II. The secondary headaches -Headache attributed to .... Part III. III. Painful cranial neuropathies, neuropathies, other facial pains, and other headaches
International Classification of Headache Disorder 2004
http://ihs-classification.org
Approach to Headache disorder
Patient presents with complaint of a headache
Critical first step: Hx taking, physical exam
Red flag signs (+)
Investigation Red flag signs or alarming signs
Meets criteria for primary headache disorder?
Migraine headache Cluster headache and other TACs
(-)
(+)
Tension-type headache Other (rare) headache disorder
Secondary headache disorder
History taking
History taking
History taking
History taking
Patient presents with complaint of a headache
Critical first step: Hx taking, physical exam
Red flag signs (+)
Investigation Red flag signs or alarming signs
Meets criteria for primary headache disorder?
Migraine headache Cluster headache and other TACs
(-)
(+)
Tension-type headache Other (rare) headache disorder
Secondary headache disorder
Alarming signs and symptoms
• “Alarming s/s suggest the possibility of secondary headache
• The studies • Headache sample (specific or nonspecific)
• Pool analyzed data => guideline
Abnormal neurological examination
Focal neurologic s/s other than typical visual or sensory aura Papilledema
Normal neurological examination Age
Age> 50
Temporal profile
Worsening headache -Mass lesion, SDH, MOH
Sudden onset -SAH, ICH, mass lesion (posterior fossa)
Neck stiffness
Concurrent event
Pregnancy, post partum -Cerebral vein thrombosis, carotid dissection, pituitary apoplexy
Headache with cancer, HIV, systemic illness (fever, arteritis, collagen vascular disease)
Provoking activity
Triggered by cough, exertion or Valsava Valsava -SAH, mass lesion
Worse in i n the morning -IICP
Worse on awakening -Low CSF pressure
Migraine
Population-based study Only migraine without aura Only migraine with aura Both types
Migraine without aura is more common (previously called common migraine) Launer LJ et al. Neurology 1999;53:537-42 1999;53:537-42
Clinical Picture Genetic Trigger factors
Environmental factors Migraine attack
Migraine triggers Diet
• • • •
Hunger Alcohol
• •
Additives
Menstruation
Sleep (too much or too little) Schedule change
Environmental factors
Certain foods
Hormonal change
•
Chronobiologic
• • • •
Light glare
Physical exertion
• •
Exercise Sex
Stress and anxiety
Odors Altitude Weather change
Head trauma
The “Classic” Migraine = Migraine with aura
‘‘Teichopsia’’ (Greek for ‘‘town wall vision’’)
‘‘On a distinct form of transient hemiopsia’’ by Dr. Dr. Hubert Airy in 1870. 1 870.
Migraine without aura
Migraine with typical aura needs 2 attacks In children, the attack may last 1-72 hours ICHD-III Cephalalgia .2014 .2014
Tension-type headache
The Northern Neuroscience Centre Chiang Mai University
NNC CMU
The term “Tension-type headache” •
Previous used terms: •
•
muscular contraction headache, psychogenic headache, psychomyogenic headache, nonmigraineous headache
Term “Tension-type” •
offer the heading underlining the uncertain pathogenesis, but indicating that some kind of or muscular tension may may play a role mental or
The Northern Neuroscience Centre Chiang Mai University
Tension-type headache
NNC CMU A. At A. At least 10 episode of headache B. Lasting B. Lasting from 30 minutes to 7 days
Episodic infrequent vs frequent Chronic Pericranial tenderness with/without
C. At C. At least two of the following four characteristics 1. bilateral 1. bilateral location 2. pressing 2. pressing or tightening (non-pulsating) quality 3. mild 3. mild or moderate intensity 4. not aggravated by routing physical activity such as walking or climbing stairs D. Both D. Both of the following: 1. no 1. no nausea or vomiting 2. no 2. no more than one of photophobia or photophobia E. Not E. Not better accounted for by another ICHD-3 diagnosis
The Northern Neuroscience Centre Chiang Mai University
NNC CMU
Differential diagnosis issues •
•
Secondary cause •
Hypertension, metabolic, systemic, sys temic, low/high CSF, CSF, diffuse intracranial lesion, sleep apnea
•
TMJ disorder dis order,, cervicogenic cerv icogenic headache
•
Myofascial pain syndrome, fibromyalgia
Primary headache - Migraine
The Northern Neuroscience Centre Chiang Mai University
NNC CMU TTH or Migraine Mild Moderate Severe Aura Unilateral Vomiting
Bilateral Photophobia
Aggravated by activity
Nausea Throbbing Pressure
Tension-type headache
Migraine
Trige rigemina minall Auto Autonomi nomicc Cephalalgia “The most severe headache ever”
Trigeminal T rigeminal Autonomic Cephalalgia (TACs) (TACs) “A group of primary headache disorders di sorders characterized by, by, short-lasting, strictly unilateral head pain that occurs in association with ipsilateral cranial autonomic features” • Cluster Headache (CH) • Paroxysmal Hemicrania (HC) • Short-lasting unilateral neuralgiform headache attack with conjunctival injection and tearing/cranial autonomic features (SUNCT/SUNA) Hemicrania Continua (HC)
!
ICHD-III Beta 2013
ICHD-II 2004 CH criteria
ICHD-III Beta 2013 CH criteria
ICHD-II ICHD-III Beta
TACs subtypes
“Longer name, shorter duration”
Prevalence
56/100,000
Very rare not known
Very rare not known
International Classification of Headache Disorder-2004 Part 1. 1. The primary headaches - Migraine, TTH, CH and other TACs, and other primary headache disorder Part II. II. The secondary headaches -Headache attributed to .... Part III. III. Painful cranial neuropathies, neuropathies, other facial pains, and other headaches
International Classification of Headache Disorder 2014
http://ihs-classification.org
Cranial Neuralgias • The presence of sudden, sharp, aching, lancinating, burning, and stabbing pain lasting from only a few seconds to less than 2 min and recurring repeatedly within short periods of time, which is often triggered by sensory or mechanical stimuli
ICHD-III beta
Trigeminal Neuralgia
•
70% of patients are older than 60 years at onset
•
Clinical hallmark:
• • • •
brief electric shock-like pains abrupt in onset and termination limited to the distributions of the trigeminal nerve commonly stimuli: mechanical
Classical trigeminal neuralgia
Symptomatic trigeminal neuralgia “TN caused by a demonstrable structural lesion”
Vertigo/Dizziness
Syndrome of vertigo: base on connection Major symptoms
• Psychiatric symptoms:
• Vertigenous sensation
• Fear
• Imbalance • Nystagmus and oscillopsia
• Anxiety • Hyperventilation syndrome
• Autonomic dysfunction
• Phobia
• N/V • Palpitation • Fluctuation in BP
Causes of vertigo Peripheral vertigo • Infection/inflammation – Peripheral vestibulopathy Vestibular Vestibular neuritis, acute neurolabyrinthitis Localized: CN7+8 affected: Ramsay Hunt syndrome Systemic: mump, measle, IM, URI
• • • •
Trauma: Trauma: post-traumatic vertigo Local tumor Vascular: rare Metabolic/ toxic – Aminoglycoside(rare)
• Other: BPPV, Meniere’s disease
Central vertigo Common is • Tumor: CP angle tumor • Demyelinating: MS • Vascular: ischemia(VBI) • Posterior fossa lesion • Migraine • Vertigenous epilepsy
Systemic causes of vertigo and dizziness • Drugs – AED, hypnotic, alcohol, analgesic
• Hypotension, presyncope • Infectious disease – Syphilis, viral, systemic infection
• Endocrine disease – Diabetes, hypothyroidism
• Vasculitis • Others: hematological, granulomatous disease, systemic toxin
Time course-onset Lasting for day or longer • Peripheral: vestibular neuritis • Central: brainstem stroke, MS
Lasting for hours or minute • Peri Peripher pheral: al: Meni Meniere’ ere’s s disease disease • Cent Central: ral: TIA TIA,, migrain migraine, e, seizur seizure e
Lasting for second • Per Periph iphera eral: l: BP BPPV PV
Vermis syndrome
BPPV
Surat Tanprawate, MD, MSc(Lond.), FRCP(T) CertHE(Hist Med) Neurology staff, Division of Neurology, CMU The Northern Neuroscience Center, CMU FB: openneurons
Thank You for Your Kind Attention
