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«Previous article | Next article»

The diagnosis of migraine and managing the disease

Dr Edward O'Sullivan — Clinical Director of the Migraine Clinic in Cork University Hospital — outlines the types of migraine headache and how they affect patients' lives

Migraine is a common neurological disorder characterised by recurrent bouts of severe headache with autonomic and neurological symptoms. In clinical practice it varies from being an infrequent episodic disorder in some patients to a condition which becomes progressive and occurs on a daily or near daily basis in others.

The clinical presentation, frequency, severity, duration and disability of attacks varies, and results in the diagnosis being straightforward in some patients, whilst in others it goes undiagnosed and undetected throughout their lives.

Epidemiology and impact
The prevalence of migraine worldwide is 10-12 per cent and it is three times more common in women. The rapid rise in the incidence of migraine in women at the time of menarche is hormonally (oestrogen) influenced and this female: male domination of 3: 1 continues throughout adult life.

The average migraine patient suffers one to two attacks per month whilst 10 per cent of migraneurs develop a progressive form and experience attacks on a daily or near daily basis.

The impact and severity of migraine helps distinguish migraine from other benign disorders.

The average patient loses three to five days from work annually. It has a huge impact personally in that patients are typically unable to function and need to lie down in a quiet dark room.

As a result, hundreds of millions of euro are lost annually from the Exchequer due to decreased productivity.

Migraine continues to be a hidden disability with only ~ 50 per cent ever being clinically diagnosed by a physician.

Clinical features
The International Headache Society has classified migraine into variety of presentations. The overwhelming number of attacks are either (1) migraine with aura (20-25 per cent) and (2) migraine without aura (~80 per cent). Rare forms of migraine are hemiplegic migraine, retinal migraine and migraine equivalents (migraine aura without headache).

The phases of a migraine attack are divided into 5 clinical phases: (a) prodromal, (b) aura, © headache phase (d) resolution and (e) recovery phase.

Prodromal Symptoms: Prior to the headache ~ 40 per cent of patients complain of prodromal or ‘warning’ symptoms which include loss of appetite or craving for certain foods, change of mood, tiredness and yawning, a heightened perception of heat and cold and fluid retention.

Aura: The aura is defined as transient, focal, reversible neurological symptom which last from five to 60 minutes. It usually precedes the headache but may coincide and continue into the headache and occurs in ~ 20 per cent of patients. By far the commonest aura symptom is visual and is described as a fortification spectra, expanding scotoma and zig-zag lines.

Other aura symptoms are: sensory (numbness or ‘pins and needles’), motor and dysphasia.

Headache Phase: The headache phase lasts from four to 72 hours and on average it lasts 24 hours. The headache may be either gradual or abrupt in onset. A typical attack has the following clinical features:

1. A unilateral headache which can be localised or extend from the frontal to the occipital regions. It is one-sided in 70 per cent of attacks and may switch sides during the attack. Thirty per cent of attacks are bilateral in location.
2. The headache is throbbing and pounding in character and exacerbated by movement.
3. The headache is severe.
4. Eighty per cent of patients complain of nausea that leads to vomiting in 50 per cent. In some patients vomiting will provide relief from the headache and many migraneurs will induce vomiting to hasten the resolution of symptoms.
5. Photophobia and phonophobia.
6. Cutaneous alloydynia at the location of the headache.

Resolution and Recovery Phase: After the headache phase most patients continue to feel tired, physically drained with a ‘washout’ feeling and require a further period of rest and sleep before they are recovered from an attack. Paradoxically a minority of patients feel euphoric, energetic and can return to normal life within a short time.

Pathophysiology of Mi-graine: The aura and headache phases of a migraine attack have separate and distinct underlying mechanisms. The aura is caused by cortical spreading depression (CSD) and the headache by activation of the trigeminovascular system.

Cortical Spreading Depression: Either spontane-ously or on exposure to a trigger factor, patients with a reduced threshold have an increased susceptibility to hyperexcitability of cortical neurons in the visual cortex located in the occiput.

This in turn leads to a self propagating wave of depolarisation across the cerebral cortex at a rate of 2-3mm / min and results in the emergence of the visual symptoms and subsequently the sensory, dysphasic and motor symptoms as the depolarising wave reaches these functional anatomical areas. The aura symptoms follow each other in keeping with the underlying mechanism.

Trigeminovascular System: The intracranial pain sensitive structures are the proximal intracerebral arteries, meningeal arteries, meninges and the large dural venous sinuses. The pain sensitive nerve innervating these structures is the ophthalmic division of the trigeminal nerve and C2.

Activation of the trigeminovascular system causes the ophthalmic division to depolarise and results in a retrograde release of neuropeptides (CGRP, neurokinin and substance P) from the peripheral end of the nerve. These neuropeptides cause local vascular effects and give rise to a neurgenic inflammatory reaction in the wall of the meningeal arteries and meninges. This further stimulates painful receptors located in these structures and pain sensitive afferent information is relayed along the trigeminal nerve where it synapses with the trigeminal nucleus caudalis in the brain stem.

Second-order neurons relay this information via the quintothalamic tract to the thalamus. Finally, third-order neurons further relay this information to the higher cortical centres where pain is perceived.

Management
Guidance principles of migraine management include:
(1) Reassurance and explan-ation of migraine.
(2) The use of headache diaries. A headache diary is an invaluable tool in migraine management. It creates objectivity and yields invaluable information regarding the frequency, severity, duration and symptomatology of attacks. It aids in the identification of trigger factors and monitors the efficacy of both the acute and preventative therapies.
(3) The avoidance of trigger factors.
(4) Acute therapies.
(5) Preventative therapies.
(6) Non-drug therapies.

Trigger Factors: Triggers are identifiable in ~ 40 per cent of patients, indicating that many attacks occur spontaneously without their being a precipitating cause. Trigger factors include: dietary (cheese, chocolate, foods containing MSG and aspirate), alcohol, stress, menstrual cycle, OCP, strong odours and environmental factors.

Acute Therapies: All acute therapies are best taken as early as possible during the headache phase, and to delay taking them at this point makes them less effective. Simple analgesics (paracetamol or aspirin), paracetamol/codeine and NSAIDs provide relief in approximately 30 per cent of migraneurs and many patients are able to successfully manage their own migraine. Their mode of action is through anti-prostaglandin actions.

The specific acute anti-migraine therapies are known as the triptans. These agents are 5-HT1B/1D receptor agonists and include sumatriptan, zolmitriptan, almotriptan, frovatriptan, eletriptan and naratriptan. The triptans have a high affinity for the 1B receptors located on the meningeal and proximal intracerebral arteries and they vasoconstrict the dilated intracranial arteries during the acute attack.

In addition, the triptans also have a high affinity for the 1D receptors located on the peripheral end of the trigeminal nerve thereby blocking the release of the neuropeptides (CGRP, neurokinin and substance P) from these terminals.

The triptans have an efficacy of 60-80 per cent and ideally provide relief within two hours. About 40 per cent of patients get a recurrence of the headache within 24 hours and will therefore require taking additional doses.

Preventative Therapies: The objectives in migraine prophylaxis are a reduction in the frequency, severity and duration of attacks. This results in reduced disability and lessens the reliance on acute therapies. In practice, only 13 per cent of migraneurs have been prescribed a preventive therapy indicating that they are underutilised.

Patients need to continue to take the medication for at least 2-3 months before efficacy can be accurately evaluated. A common mistake is for patients to discontinue the medication within a few weeks. Most of the preventive therapies were discovered through serendipitous use and these include beta-blockers (propanolol, atenolol), anti-epileptics (sodium valproate) and antidepressants (amitriptyline, SSRI). The best clinical trials are conducted with topiramate, which determined the end-point evaluations outlined above.

Other preventative drugs include: pizotifen and sibellium.

The mechanisms of actions of the preventive therapies are poorly understood but are thought to confer benefit through inhibition of cortical spreading depression (CSD) through stabilisation of Na+, K+ and Ca+ channels. In addition they act on adrenergic and noradrenergic pathways, inhibit the actions of glutamate and enhance the role of GABA receptor actions.

Future Developments: There are at present a number of new generation acute and preventive therapies in late-stage clinical development.

The most promising of the acute therapies are the CGRP antagonists (telcagepant), which in clinical trials show a similar efficacy to the triptans without having vascular vasoconstriction actions.

This is important as the triptans are contraindicated in patients with ischaemic heart disease and uncontrolled hypertension.

Tonabersat is a novel preventive therapy which inhibits cortical spreading depression and in turn inhibits nitric oxidase production and trigeminovascular activation. The results of a recent clinical trial only showed a marginal improvement over placebo. Nevertheless further clinical trials are on-going with a number of different end-points being evaluated.

Dr Edward M. O’Sullivan, Clinical Director Headache / Migraine Clinic, Cork University Hospital and GP, Cork City.

The Migraine Association of Ireland will be holding an information meeting this weekend in the Bracken Court Hotel, Balbriggan (Sunday, November 29, 2.00 pm). The keynote speaker is Specialist Migraine Nurse, Esther Tomkins.
Further details at the Migraine Association’s helpline at 1850 200 378 or at info@ migraine.ie

Posted in Eye, Ear, Nose & Throat on 26 November 2009
Tags: migraine

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abortion, accupuncture, ACE inhibitors, acne, ADHD, alcohol, allergies, Alzheimer's, anaemia, anaethesia, anorexia, antibiotics, antidepressants, antihistamine, anxiety, appetite control, arthritis, ASCOT, aspirin, asthma, atherosclerosis, autism, autoantibodies, back pain, beta carotene, beta-blockers, bipolar disorder, birth, bleeding, blindness, blood pressure, body dysmorphic disorder, body mass, breast cancer, breast feeding, bronchitis, Caesarean section, calcium, cancer, carcinogens, carcinoma, cardiac syncope, cardiolgy, cataracts, cervical cancer, chemotherapy, child psychiatry, children, cholesterol, clinical trial, clopidogrel, Clostridium difficile, cognitive behavioural therapy, colectomy, colic, colorectal cancer, complementary and alternative therapies, contraception, COPD, coronary care, coronary stents, Crohn's, cystic fibrosis, defibrillator, dementia, depression, dermatology, diabetes management, diet, disability, DNA, Down's syndrome, eating disorders, echinacea, ECT, eczema, elderly people, endoscopy, epilepsy, erectile dysfunction, euthanasia, exercise, fat, fertility, fitness, flu pandemic, fluoxetine, folic acid, food labelling, fracture, fragile X syndrome, general surgery, genetics, gerontology, GIK infusion therapy, GORD, gout, haemodialysis, hearing, heart attack, heart disease, heart failure, heart health, hepatitis, HIV, hospital care, HPV, HRT, hyperglycaemia, hypertension, hypoglycaemia, IBD, ICU, incontinence, infant, infant mortality, infection, inflammatory bowel disease, influenza, invasive candidiasis, IQ, Irish Heart Foundation, irritable bowel syndrome, keyhole surgery, kidney disease, laser, learning difficulties, leukaemia, liver disease, lumbar disk herniation, lung cancer, lung disease, lymph nodes, macular degeneration, macular oedema, magnetic resonance imaging (MRI), malaria, malnutrition, Marfan syndrome, media, medical ethics, medical research, medication, meningitis, mental illness, metabolic syndrome, migraine, miscarriage, mortality rate, MRSA, multiple sclerosis (MS), NCHDs, nephrology, neurology, OAB, obesity, obstetrics, occupational health, ocular medicine, omega-3, opthalmology, oral cancer, organ transplantation, orthopaedics, osteoporosis, otolaryngology, ovarian cancer, paediatrics, pain management, pancreatic cancer, panic, Parkinson’s disease, patient safety, patient-physician communication, personality disorders, physiotherapy, plastic surgery, polio, practice, pre-eclampsia, pregnancy, preventative health care, probiotics, prostate cancer, psoriasis, psychiatric admission, psychiatry, psychotherapy, PTSD, public health, quality of life, radiology, radiotherapy, rectal cancer, reproductive health, research, resuscitation, rheumatoid arthritis, rheumatology, rhinitis, salt, SARS, schizophrenia, screening, seizures, self harm, sexual abuse, sexual health, sexually transmitted infections, SGA, sinusitis, skin cancer, sleep disorders, smoking, smoking ban, spinal injury, sports medicine, statins, stress, stroke, substance abuse, suicide, supplement, surgery, syncope, technology, teenagers, testosterone, thoracic surgery, thrombosis, thyroid cancer, tonsillectomy, tonsillitis, Tourette's syndrome, toxicology, travel medicine, tuberculosis, tumour angiogenesis, type 1 diabetes, type 2 diabetes, ulcer, ulcerative colitis, urinary incontinence, vaccine, vitamins, weight, WHO, women's health, World Health Assembly

«Previous article | Next article»

The diagnosis of migraine and managing the disease

Dr Edward O'Sullivan — Clinical Director of the Migraine Clinic in Cork University Hospital — outlines the types of migraine headache and how they affect patients' lives

Migraine is a common neurological disorder characterised by recurrent bouts of severe headache with autonomic and neurological symptoms. In clinical practice it varies from being an infrequent episodic disorder in some patients to a condition which becomes progressive and occurs on a daily or near daily basis in others.

The clinical presentation, frequency, severity, duration and disability of attacks varies, and results in the diagnosis being straightforward in some patients, whilst in others it goes undiagnosed and undetected throughout their lives.

Epidemiology and impact
The prevalence of migraine worldwide is 10-12 per cent and it is three times more common in women. The rapid rise in the incidence of migraine in women at the time of menarche is hormonally (oestrogen) influenced and this female: male domination of 3: 1 continues throughout adult life.

The average migraine patient suffers one to two attacks per month whilst 10 per cent of migraneurs develop a progressive form and experience attacks on a daily or near daily basis.

The impact and severity of migraine helps distinguish migraine from other benign disorders.

The average patient loses three to five days from work annually. It has a huge impact personally in that patients are typically unable to function and need to lie down in a quiet dark room.

As a result, hundreds of millions of euro are lost annually from the Exchequer due to decreased productivity.

Migraine continues to be a hidden disability with only ~ 50 per cent ever being clinically diagnosed by a physician.

Clinical features
The International Headache Society has classified migraine into variety of presentations. The overwhelming number of attacks are either (1) migraine with aura (20-25 per cent) and (2) migraine without aura (~80 per cent). Rare forms of migraine are hemiplegic migraine, retinal migraine and migraine equivalents (migraine aura without headache).

The phases of a migraine attack are divided into 5 clinical phases: (a) prodromal, (b) aura, © headache phase (d) resolution and (e) recovery phase.

Prodromal Symptoms: Prior to the headache ~ 40 per cent of patients complain of prodromal or ‘warning’ symptoms which include loss of appetite or craving for certain foods, change of mood, tiredness and yawning, a heightened perception of heat and cold and fluid retention.

Aura: The aura is defined as transient, focal, reversible neurological symptom which last from five to 60 minutes. It usually precedes the headache but may coincide and continue into the headache and occurs in ~ 20 per cent of patients. By far the commonest aura symptom is visual and is described as a fortification spectra, expanding scotoma and zig-zag lines.

Other aura symptoms are: sensory (numbness or ‘pins and needles’), motor and dysphasia.

Headache Phase: The headache phase lasts from four to 72 hours and on average it lasts 24 hours. The headache may be either gradual or abrupt in onset. A typical attack has the following clinical features:

1. A unilateral headache which can be localised or extend from the frontal to the occipital regions. It is one-sided in 70 per cent of attacks and may switch sides during the attack. Thirty per cent of attacks are bilateral in location.
2. The headache is throbbing and pounding in character and exacerbated by movement.
3. The headache is severe.
4. Eighty per cent of patients complain of nausea that leads to vomiting in 50 per cent. In some patients vomiting will provide relief from the headache and many migraneurs will induce vomiting to hasten the resolution of symptoms.
5. Photophobia and phonophobia.
6. Cutaneous alloydynia at the location of the headache.

Resolution and Recovery Phase: After the headache phase most patients continue to feel tired, physically drained with a ‘washout’ feeling and require a further period of rest and sleep before they are recovered from an attack. Paradoxically a minority of patients feel euphoric, energetic and can return to normal life within a short time.

Pathophysiology of Mi-graine: The aura and headache phases of a migraine attack have separate and distinct underlying mechanisms. The aura is caused by cortical spreading depression (CSD) and the headache by activation of the trigeminovascular system.

Cortical Spreading Depression: Either spontane-ously or on exposure to a trigger factor, patients with a reduced threshold have an increased susceptibility to hyperexcitability of cortical neurons in the visual cortex located in the occiput.

This in turn leads to a self propagating wave of depolarisation across the cerebral cortex at a rate of 2-3mm / min and results in the emergence of the visual symptoms and subsequently the sensory, dysphasic and motor symptoms as the depolarising wave reaches these functional anatomical areas. The aura symptoms follow each other in keeping with the underlying mechanism.

Trigeminovascular System: The intracranial pain sensitive structures are the proximal intracerebral arteries, meningeal arteries, meninges and the large dural venous sinuses. The pain sensitive nerve innervating these structures is the ophthalmic division of the trigeminal nerve and C2.

Activation of the trigeminovascular system causes the ophthalmic division to depolarise and results in a retrograde release of neuropeptides (CGRP, neurokinin and substance P) from the peripheral end of the nerve. These neuropeptides cause local vascular effects and give rise to a neurgenic inflammatory reaction in the wall of the meningeal arteries and meninges. This further stimulates painful receptors located in these structures and pain sensitive afferent information is relayed along the trigeminal nerve where it synapses with the trigeminal nucleus caudalis in the brain stem.

Second-order neurons relay this information via the quintothalamic tract to the thalamus. Finally, third-order neurons further relay this information to the higher cortical centres where pain is perceived.

Management
Guidance principles of migraine management include:
(1) Reassurance and explan-ation of migraine.
(2) The use of headache diaries. A headache diary is an invaluable tool in migraine management. It creates objectivity and yields invaluable information regarding the frequency, severity, duration and symptomatology of attacks. It aids in the identification of trigger factors and monitors the efficacy of both the acute and preventative therapies.
(3) The avoidance of trigger factors.
(4) Acute therapies.
(5) Preventative therapies.
(6) Non-drug therapies.

Trigger Factors: Triggers are identifiable in ~ 40 per cent of patients, indicating that many attacks occur spontaneously without their being a precipitating cause. Trigger factors include: dietary (cheese, chocolate, foods containing MSG and aspirate), alcohol, stress, menstrual cycle, OCP, strong odours and environmental factors.

Acute Therapies: All acute therapies are best taken as early as possible during the headache phase, and to delay taking them at this point makes them less effective. Simple analgesics (paracetamol or aspirin), paracetamol/codeine and NSAIDs provide relief in approximately 30 per cent of migraneurs and many patients are able to successfully manage their own migraine. Their mode of action is through anti-prostaglandin actions.

The specific acute anti-migraine therapies are known as the triptans. These agents are 5-HT1B/1D receptor agonists and include sumatriptan, zolmitriptan, almotriptan, frovatriptan, eletriptan and naratriptan. The triptans have a high affinity for the 1B receptors located on the meningeal and proximal intracerebral arteries and they vasoconstrict the dilated intracranial arteries during the acute attack.

In addition, the triptans also have a high affinity for the 1D receptors located on the peripheral end of the trigeminal nerve thereby blocking the release of the neuropeptides (CGRP, neurokinin and substance P) from these terminals.

The triptans have an efficacy of 60-80 per cent and ideally provide relief within two hours. About 40 per cent of patients get a recurrence of the headache within 24 hours and will therefore require taking additional doses.

Preventative Therapies: The objectives in migraine prophylaxis are a reduction in the frequency, severity and duration of attacks. This results in reduced disability and lessens the reliance on acute therapies. In practice, only 13 per cent of migraneurs have been prescribed a preventive therapy indicating that they are underutilised.

Patients need to continue to take the medication for at least 2-3 months before efficacy can be accurately evaluated. A common mistake is for patients to discontinue the medication within a few weeks. Most of the preventive therapies were discovered through serendipitous use and these include beta-blockers (propanolol, atenolol), anti-epileptics (sodium valproate) and antidepressants (amitriptyline, SSRI). The best clinical trials are conducted with topiramate, which determined the end-point evaluations outlined above.

Other preventative drugs include: pizotifen and sibellium.

The mechanisms of actions of the preventive therapies are poorly understood but are thought to confer benefit through inhibition of cortical spreading depression (CSD) through stabilisation of Na+, K+ and Ca+ channels. In addition they act on adrenergic and noradrenergic pathways, inhibit the actions of glutamate and enhance the role of GABA receptor actions.

Future Developments: There are at present a number of new generation acute and preventive therapies in late-stage clinical development.

The most promising of the acute therapies are the CGRP antagonists (telcagepant), which in clinical trials show a similar efficacy to the triptans without having vascular vasoconstriction actions.

This is important as the triptans are contraindicated in patients with ischaemic heart disease and uncontrolled hypertension.

Tonabersat is a novel preventive therapy which inhibits cortical spreading depression and in turn inhibits nitric oxidase production and trigeminovascular activation. The results of a recent clinical trial only showed a marginal improvement over placebo. Nevertheless further clinical trials are on-going with a number of different end-points being evaluated.

Dr Edward M. O’Sullivan, Clinical Director Headache / Migraine Clinic, Cork University Hospital and GP, Cork City.

The Migraine Association of Ireland will be holding an information meeting this weekend in the Bracken Court Hotel, Balbriggan (Sunday, November 29, 2.00 pm). The keynote speaker is Specialist Migraine Nurse, Esther Tomkins.
Further details at the Migraine Association’s helpline at 1850 200 378 or at info@ migraine.ie

Posted in Eye, Ear, Nose & Throat on 26 November 2009
Tags: migraine