Case 8 Migraine

Description of migraine

Definition

Migraine is a complex neurovascular disorder characterised by episodic headaches. The two major categories of migraine are classic migraine (i.e. migraine with aura) and common migraine (i.e. migraine without aura). Other variants of the disorder are chronic migraine (i.e. producing ≥15 attacks per month), hemiplegic migraine (i.e. associated with defects to chromosomes 1, 2 and 19) and basilar artery migraine (i.e. caused by vertebrobasilar ischaemia).^1,²

Epidemiology

Migraine typically begins in adolescence. The prevalence of the condition increases from this point, peaking around age 40 and declining thereafter. In the US, migraine affects around eighteen per cent of women and six per cent of men.³ The higher prevalence rate reported in the female population is evident across all age groups, except for the prepubescent period, in which migraine is relatively more common in males. Migraine is also more prevalent among Caucasians, particularly Europeans and Americans; it is least prevalent in the African and Asian populations.³

The aetiology and pathophysiology of migraine are complex and still not completely understood. Genetic predisposition is likely to be a contributing factor, although not all cases have a familial tendency.⁴ Even though specific causes of migraine have yet to be established, a number of triggers have been identified. Intrinsic triggers, such as oestrogen fluctuation, brain serotonin depletion, temporomandibular joint dysfunction, emotional stress, excessive or inadequate sleep and neck pain, as well as extrinsic triggers such as tyramine-containing foods (i.e. cheese, red wine, chocolate, preserved meats), monosodium glutamate, weather changes (such as increased temperature or elevated barometric pressure), head trauma, hormone therapy, oral contraceptive use, strong odours, intense or flashing light and skipped meals, have all been associated with the onset of migraine.^1,^2,⁵ It is also suggested that nutritional deficiency, specifically, magnesium deficiency, could play a role in the pathogenesis of migraine.⁶^–⁸

Genetic predisposition and/or risk factors as yet unknown may lower an individual’s threshold to these triggers, upon exposure to which, susceptible individuals may experience a reduction in cerebral blood flow, which, in some people, may manifest as an aura. The cortical spreading depression (CSD) of blood flow from the occipital lobe to other regions of the cerebral cortex, which may be preceded by brain serotonin depletion, triggers the diffuse activation of perivascular trigeminal sensory nerves.⁵ These impulses are transmitted to the trigeminal nucleus caudalis of the brainstem and from there to the periaqueductal grey matter, sensory thalamus and sensory cortex. The stimulation of these regions results in the manifestation of pain.^2,⁴

There are several deviations from this theory, however. Some argue that the pain of migraine is simply a rebound vasodilatatory response to CSD. Others propose that the activation of the trigeminovascular system increases neuropeptide release, which results in painful inflammation to the dura mater and cranial vessels.¹ Still others have also indicated that migraine may be the result of mitochondrial dysfunction and a subsequent impairment in cellular oxygen metabolism.⁹ While researchers do not completely agree on the pathophysiology of migraine, there is general agreement that migraine is a neurovascular disorder.

Clinical manifestations

The International Headache Society (IHS) defines migraine as a repeated, episodic headache of 4–72 hours duration that is characterised by any two of the following: unilateral distribution, throbbing quality, moderate or severe intensity and/or worsened by movement. To complete the IHS criteria, the pain also should be accompanied by nausea and vomiting, or photophobia and phonophobia.⁴ It is not unusual for individuals with migraine to also experience osmophobia, poor concentration, blurred vision, clumsiness, localised weakness, numbness or tingling, irritability and scalp tenderness.^1,²

In cases of classic migraine, the headache is preceded by a temporary neurological disturbance known as an aura. This phenomenon typically presents as a visual defect (e.g. bright zigzags, scintillating lights), but may also manifest as a sensory or motor disturbance (e.g. paraesthesias, dysarthria, ataxia, confusion).² Hemiplegic migraine generally presents as unilateral weakness, and basilar artery migraine as focal weakness, vertigo, ataxia and altered consciousness.¹ The symptoms of migraine are often aggravated by bright lights, noise, strong odours and physical activity, and are somewhat relieved following seclusion in a dark, quiet environment.¹

Clinical case

35-year-old woman with classic migraine

Rapport

Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, as well as the accuracy and comprehensiveness of the clinical assessment.

Assessment

Once measures have been put into place to build client–practitioner rapport, the clinician can begin the clinical assessment.

Health history

History of presenting condition

A 35-year-old woman is referred to the clinic for complementary management of migraine. The client was diagnosed with classic migraine at the age of 17 years and has, in conjunction with her general practitioner, been managing the condition with Mersyndol Forte® (paracetamol, codeine phosphate and doxylamine succinate) and metoclopramide, and, in severe cases, with pethidine and metoclopramide. The headaches, which occur every 3–6 weeks, are preceded by a visual aura, specifically, bright zigzags, and typically last 4–6 hours. The client describes the migraine as pulsating, non-radiating and unilateral. In most cases, the pain is of moderate intensity (pain score = 6/10). The pain is almost always accompanied by nausea, photophobia, phonophobia and blurred vision, and, infrequently, by vomiting. Bright light and emotional stress often trigger the condition, but not always. The onset of migraine is not associated with the consumption of any particular foods or with any stages of the menstrual cycle. Physical activity, bright light and noise aggravate the condition. While the client obtains moderate relief of symptoms from the aforementioned analgesics and from seclusion in a dark, quiet room, these strategies are only palliative. The client is now seeking alternative treatment options to decrease the frequency and intensity of migraine in order to improve her quality of life.

Medical history

Lifestyle history

Diet and fluid intake
Breakfast	Black tea, white English muffin with butter.
Morning tea	Apple, banana, orange.
Lunch	White wrap with lettuce, cheese, chicken and avocado, quiche with mixed green salad.
Afternoon tea	Black tea, mixed nuts (e.g. almonds, cashews, Brazil nuts).
Dinner	Grilled whiting or chicken breast with steamed carrots, beans and potato au gratin, cream of chicken soup or potato and leek soup with white bread.
Fluid intake	2–4 cups of black tea a day, 2–3 cups of water a day.
Food frequency
Fruit	1–2 serves daily
Vegetables	2–4 serves daily
Dairy	2–3 serves daily
Cereals	3–4 serves daily
Red meat	0–1 serve a week
Chicken	3 serves a week
Fish	1–2 serves a week
Takeaway/fast food	0–1 time a week

Quality and duration of sleep

Interrupted sleep; has difficulty falling asleep (sleep latency of approximately 1–1.5 hours); average duration is 5–6 hours.

Frequency and duration of exercise

Drives to work. Walks the dog 1–2 times a week for 20 minutes. Engages in incidental exercise (e.g. cleaning, gardening, shopping) less than 3 hours a day and sedentary activities (e.g. desk-bound activities, television) more than 7 hours a day.

Socioeconomic background

The client was born in Canada, as was her mother. Her father was born in France. Upon completing her social work degree 13 years ago, the client moved interstate and took up residence in an inner city apartment. The client has seen very little of her parents and siblings since the move, which upsets her at times. The client works in a general hospital as a senior social worker and, while she enjoys her chosen career and the company of her work colleagues during and outside normal working hours, the work is very demanding and stressful. The client is single with no children and there are no notable religious or cultural beliefs to report.

Physical examination

Inspection

Client is alert, cooperative, appropriately dressed, well-groomed and maintains good attention and eye contact. No anomalies in coordination, posture or gait are evident during standing, sitting or ambulation. Cranial nerves I to XII are grossly intact, with extraocular muscles intact. Pupils are equal and reactive to light and accommodation, and face, palate and neck and shoulder muscles are symmetrical. There is no sign of muscular atrophy to the neck, back, shoulders, upper limbs or lower limbs.

Olfaction

There is no loss of smell or perception of abnormal odours. There is no abnormal odour to the client.

Palpation

Paranasal sinuses are non-tender. There is no tenderness to the head, neck, spine or shoulders. Range of motion of the neck, spine and shoulders is unremarkable. Peripheral sensory examination is intact to light touch and pinprick.

Percussion

All deep tendon reflexes are normal.

Auscultation

The client expresses concerns about the migraine headaches in a calm, clear, well-paced and articulate manner. There is no evidence of obsessions, compulsions, delusions, paranoid thoughts or impaired memory recall and retention. Client is oriented to time, place and person.

Additional signs

Client is afebrile (36.4°C, per oral), weight is high-normal (BMI is 24.8 kg/m², waist circumference is 75 cm) and blood pressure is high-normal (138/86).

Clinical assessment tools

Client responses to the 14 items in the migraine-specific quality of life questionnaire (MSQ v.2.1) show migraine headaches have a moderate impact on the client’s quality of life. Specifically, migraine was shown to have a modest impact on role restriction (55/100), role prevention (73/100) and emotional functioning (62/100); higher scores were indicative of greater function.

Diagnostics

CAM practitioners can request, perform and/or interpret findings from a range of diagnostic tests in order to add valuable data to the pool of clinical information. While several investigations are pertinent to this case (as described below), the decision to use these tests should be considered alongside factors such as cost, convenience, comfort, turnaround time, access, practitioner competence and scope of practice, and history of previous investigations.

Pathology tests

Magnesium deficiency test

Magnesium deficiency may be implicated in the pathogenesis of migraine.⁶^–⁸ Intracellular and/or extracellular magnesium concentration may be measured using a range of different specimens – hair, erythrocytes, serum, urine and faeces. While some authorities indicate that erythrocytic magnesium concentration may be more sensitive than other methods in measuring magnesium levels,¹⁰ there has been little rigorous research to substantiate this argument. In fact, studies suggest that hair magnesium may be a more sensitive measure of magnesium concentration than erythrocytic magnesium, and serum magnesium the least sensitive.¹¹ Thus, assessing hair or erythrocytic magnesium concentration may help to determine whether magnesium deficiency is a contributing factor in this condition.

Radiology tests

X-ray, CT, MRI and/or PET are indicated only if the migraine is believed to be caused by an underlying condition, such as stroke, chronic sinusitis, vertebral anomaly, or space-occupying lesion.

Functional tests

Not applicable.

Invasive tests

Invasive tests are not usually required for a diagnosis of migraine unless serious underlying pathology is a suspected cause of the migraine, in which case a lumbar puncture may be performed to rule out conditions such as encephalitis or meningitis.

Miscellaneous tests

Electroencephalogram (EEG) measures the electrical activity of the brain by placing electrodes on an individual’s scalp. The abnormal frequency, characteristics and amplitude of these brain wave patterns, either at rest or following stimulation, may indicate the presence and location of epilepsy. An EEG may be indicated if epilepsy is believed to be masquerading as migraine.¹²

Diagnosis

Clusters of data extracted from the health history, clinical examination and pertinent diagnostic test results point towards the following differential CAM diagnosis.

• Headache (actual), secondary to classic migraine, related to genetic predisposition (client’s mother has a history of migraine), emotional stress (client is employed in a stressful occupation, and is often upset by the lack of contact with her family), inadequate sleep (client reports poor-quality sleep, including an interrupted sleep pattern, long sleep latency and short sleep duration), bright lights (client identifies bright lights as being a trigger of migraine), magnesium deficiency (magnesium deficiency may predispose a person to migraine attacks; the client regularly consumes alcohol and caffeine, which can decrease magnesium absorption and increase urinary excretion; this should be confirmed by measuring hair/red blood cell (RBC) magnesium concentration), and food intolerance (client frequently consumes high tyramine-containing foods such as red wine and cheese – these foods may trigger migraine attacks in susceptible individuals).

Planning

The goals and expected outcomes that best serve the client’s needs, and are most relevant to this case (as determined by the clinical assessment and CAM diagnoses), are as follows.

Goals

1. Client will report an improvement in migraine headaches (client is seeking a reduction in the frequency and intensity of migraine attacks).

2. Client will demonstrate an improvement in migraine-specific quality of life (client is seeking an improvement in her quality of life).

Application

The range of interventions reported in the CAM literature that may be used in the treatment of migraine are appraised below.

Diet

Low antigenic diet (Level II, Strength C, Direction + (for oligoantigenic diet only))

Tyramine-containing foods, such as cheese, red wine, chocolate and preserved meats, and food additives such as monosodium glutamate, are considered to be key dietary triggers of migraine headache.^1,² Even though many studies have explored the relationship between these triggers and the onset of migraine, the evidence is not convincing. Several dietary studies have, for instance, reported a large reduction in migraine frequency during the consumption of an oligoantigenic diet and the provocation of migraine attacks following double-blind challenges with suspected dietary triggers.¹⁸^–²⁰ These findings should be considered with caution given the small size of the studies and the lack of corroborating evidence from larger trials.

Several controlled clinical trials have also demonstrated an increased incidence of migraine attacks following the consumption of low tyramine-containing red wine ²¹ and aspartame²² when compared with controls, but many studies have failed to find a statistically significant difference in migraine frequency in groups receiving tyramine,²³ chocolate²⁴ or a low vasoactive amine diet²⁵ when compared with controls. This is corroborated by findings from a systematic review of 10 RCTs exploring the relationship between oral ingestion of biogenic amines and food intolerance reactions.²⁶ The discrepancies between these research findings and those reported in the professional literature need to be resolved to minimise clinician confusion about the best practice care of migraine.

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue