Headache

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  • Tension-type headache
    • This is the most common type of headache
    • Emotional strain or anxiety is a common precipitant to tension-type headache
    • The pain of tension headache is usually constant and generalised but often radiates forward from the occipital region.
    • It is described as ‘dull’, ‘tight’ or like a ‘pressure’, and there may be a sensation of a band round the head or pressure at the vertex.
    • In contrast to migraine, the pain may continue for weeks or months without interruption
    • there is no associated vomiting or photophobia.
    • The patient can usually continue normal activities, and the pain may be less noticeable when the patient is occupied.
    • The pain is characteristically less severe in the early part of the day and becomes more troublesome as the day goes on.
    • Local tenderness may be present over the skull vault or in the occiput but this should be distinguished from the acute pain precipitated by skin contact in trigeminal neuralgia and the exquisite tenderness of temporal arteritis. Typically, the headache does not respond well to treatment with analgesics.
    • Management
      • Physiotherapy (with muscle relaxation and stress management) is usually bene- ficial
      • low-dose amitriptyline sometimes helps.
  • Migraine
    • affects about 20% of females and 6% of males at some point in life.
    • Migraine usually presents before the age of 40
    • Pathophysiology
      • Aura is due to dysfunction of ion channels which leads to a spreading front of cortical depolarisation (excitation) followed by hyperpolarisation (depression of activity).
      • Family history is common in migraine
      • contraceptive pill does appear to exacerbate migraine in many patients, and to increase the small risk of stroke in patients who suffer from migraine with aura.
      • In some patients there are identifiable dietary precipitants such as cheese, chocolate or red wine.
      • When psychological stress is involved, the migraine attack often occurs after the period of stress, so that some patients tend to have attacks at weekends or at the beginning of a holiday.
      • The headache is associated with vasodilatation of extracranial vessels
    • Clinical features
      • Migraine presents with a symptom triad of
        • paroxysmal headache
        • nausea and/or vomiting
        • ‘aura’ of focal neurological events (usually visual).

 

 

  • ‘classical’ migraine versus ‘common’ migraine
  • Patients with all three of these features are said to have migraine with aura (‘classical’ migraine).
  • Those with paroxysmal headache (with or without vomiting) but no ‘aura’ are said to have migraine without aura (‘common’ migraine).
        • A classical migraine attack starts with a non-specific pro- drome of malaise and irritability followed by the aura of a focal neurological event, and then a severe, throbbing, hemicranial headache with photophobia and vomiting.
        • During the headache phase, patients prefer to be in a quiet, darkened room and to sleep.
        • The headache may persist for several days.
        • The aura most often takes the form of fortification spectra, which are shimmering, silvery zigzag lines which march across the visual fields over a period of about 20 minutes, sometimes leaving a trail of temporary visual field loss.
        • In some patients there is a sensory aura which is a spreading front of tingling followed by numbness which moves, over 20–30 minutes, from one part of the body to another.
        • If the dominant hemisphere is involved, the patient may also experience transient aphasia.
        • Limb weakness can occur in migraine and is termed hemiplegic migraine.
        • In some patients the focal events may occur by themselves (‘migraine equivalent’
        • In a smaller number of patients, the symptoms of the aura do not resolve, leaving more permanent neurological disturbance (‘complicated migraine’).
  • Management
  • Treatment of an acute attack consists of simple analgesia with aspirin or paracetamol, often combined with an antiemetic such as metoclopramide or domperidone.
  • Long-term use of codeine-containing analgesic preparations should be avoided.
  • Severe attacks can be treated with one of the ‘triptans’ (e.g. sumatriptan),
  • 5-HT agonists that are potent vasoconstrictors of the extracranial arteries.
                • These can be administered orally, sublingually, by subcutaneous injection or by nasal spray.
  • Ergotamine preparations should be avoided since they easily lead to dependence.
  • dependence is less likely to happen with the triptans, but it can occur.
  • If attacks are frequent, they can often be prevented with propranolol , tricyclic such as amitriptyline , sodium valproate  or topiramate

 

Cluster headache

  • Cluster headaches (also known as migrainous neuralgia)
  • 10–50 times less common than migraine.
  • There is a 5:1 predominance of males and onset is usually in the third decade.
  • Pathophysiology
    • there are no provoking dietary factors and there is a male predominance.
    • Patients are usually heavy smokers with a higher than average alcohol consumption.
  • Clinical features
    • The characteristic presentation is with periodic, severe, unilateral periorbital pain accompanied by unilateral lacrimation, nasal congestion and conjunctival injection, often with the other features of Horner’s syndrome.
    • The pain, whilst being very severe, is characteristically brief (30–90 minutes). Typically, the patient develops these symptoms at a particular time of day (often in the early hours of the morning).
    • The syndrome may occur repeatedly for a number of weeks, followed by a respite for a number of months before another cluster occurs.
  • Management
    • Acute attacks can usually be halted by subcutaneous injections of sumatriptan or by inhalation of 100% oxygen
    • other migraine therapies are ineffective
    • Preventative therapy with the agents used for migraine is often ineffective
    • Attacks can be prevented in some patients by verapamil (80–120mg 8-hourly), methysergide or short courses of oral corticosteroids.
    • Patients with severe and debilitating clusters can be helped with lithium therapy,

 

Trigeminal neuralgia

  • This is characterised by lancinating pain in the second and third divisions of the trigeminal nerve territory
  • usually in patients over the age of 50 years.
  • Pathophysiology
    • Trigeminal neuralgia is thought to be caused by an aberrant loop of the cerebellar arteries compressing the trigeminal nerve as it enters the brain stem.
    • When trigeminal neuralgia occurs in multiple sclerosis, there is a plaque of demyelination in the trigeminal root entry zone.
  • Clinical features
    • The pain is severe and very brief but repetitive, causing the patient to flinch as if with a motor tic (hence the French term for the condition, ‘tic douloureux’).
    • It may be precipitated by touching trigger zones within the trigeminal territory, by cold wind blowing on the face, or by eating.
    • Physical signs are usually absent.
    • There is a tendency for the condition to remit and relapse over many years.
  • Management
    • The pain usually responds to carbamazepine
    • In patients who cannot tolerate carbamazepine, gabapentin or pregabalin may be effective.
    • Various surgical treatments
    • injection of alcohol or phenol into a peripheral branch of the nerve.
    • Probably more effective is making a radiofrequency lesion in the nerve near the Gasserian ganglion.
    • Alternatively, the vascular compression of the trigeminal nerve can be relieved through a posterior craniotomy, often with substantial success. This approach is usually favoured in younger patients .

What Causes Headaches?
What causes headaches? There are many different types of headache including migraines, ocular migraines, cluster headaches, sinus headaches and tension headaches

Headaches – Mechanical and Nutritional Causes of Headache Pain

Acupressure for Headache Relief

What is migraine?
Migraine is more than just a headache.

Migraine Pathophysiology

Migraine Mechanism