Thursday, January 12, 2017

The basics: Migraine

Hey Awesomites!
Lets understand the basics of migraine here-

Migraine was thought to be a vascular disorder since decades with headache attributed solely to dilation and inflammation of extra- cranial arteries within the pain- producing intracranial meningeal structures. The role of external carotid artery vasculature in migraine headache has been explained in the past decade. But the recent evidences suggest the involvement of both, vascular and neuronal components in the pathogenesis of migraine attack.
Activation of meningeal afferents, neuropeptide release and neurogenic inflammation play a pivotal role in the generation of pain in migraine headache.

Neurogenic inflammation-
Activation of the primary afferent neurons by the disease process or primodal nociceptive receptors on peripheral nerve terminals generate axon reflexes which lead to 'retrograde' release of pro-inflammatory neuropeptides.
These peptides interact with endothelial, mast and immune cells and the vascular smooth muscles to result in:
             - erythema and hyperemia (secondary to local vasodilation).
             - local edema (secondary to plasma- protein extravasation).
             - hypersensitivity (due to alterations in excitability of sensory neurons).
This phenomenon is referred to as neurogenic inflammation.

This disorder is believed to be influenced by a mixture of environmental and genetic factors. About two- thirds of cases run in families. Females are affected more than men (except girls in pre-pubertal age group and women after menopause). This trend in its occurrence suggests a role of change in hormonal levels (especially oestrogen) in the pathogenesis of the disease.

Clinical features-
Migraine is characterised by a triad of major symptoms (mnemonic PAiN):-
                  - Paroxysmal headache: recurrent, intense throbbing pain on one side of head.
                  - Aura: perceptual disturbance with a series of focal neurological events
                  - Nausea and vomiting

Types of migraine:- (two major)
1. Classical migraine (migraine with aura)- the patient presents with all the above three symptoms.
2. Common migraine (migraine without aura)- the patient has paroxysmal headache with a feeling of nausea and vomiting but no aura.

Other types:-
- Migraine without headache
- Migraine with brainstem aura (Basilar- type)
- Hemiplegic migraine (familial and sporadic)
- Retinal migraine (rare)
- Chronic migraine (episodes of headache occuring on 15 days per month for more than 3 months).

☆ Classical migraine attack-
There are 4 phases of a classical migraine attack:-

1. Prodrome phase (hours or days before the attack; occurs in 30-40% patients) with the symptoms of malaise, aphasia, increased urination, neck pain, sleepiness etc.

2. Phase of Aura (occurs in 25-30% patients) with the following symptoms: (mnemonic- 4As)
                        - Alice in wonderland syndrome
                        - Allodynia
                        - Aphasia
                        - Auditory and olfactory hallucinations
       Visual symptoms in the phase of aura: the patient notices a faint/ dim glow of light and then silvery zig- zag lines (shimmering effect) which progresses across the visual field over 20 minutes.

☆ Sensory aura (in 10% of migraineurs)- is a spreading front of electrical stimulation followed by depression of activity of cortical cells (Cortical spreading depression) presented by the patient as a tingling sensation followed by numbness which moves from one part of body to another over 20-30 minutes.

3. Migraine headache (unilateral; may shift to the other side) worsened on physical exercise
              - pulsatile dilation of extracranial vessels is the immediate cause of pain.
              - may occur for 4-72 hours in adults and 1-72 hours in children depending upon severity.
              - Pain occurs in the affected area (eyes, sinus area, teeth and jaw).
              - Other symptoms- confusion, mood disoders, dehydration and fluid retention, hot flashes, osmophobia, phonophobia, photophobia, vertigo etc.

4. Postdrome phase (hours to days after headache) with symptoms of fatigue, low intellect levels, depression, etc.

Drug therapy of migraine:- depends upon the severity of migraine attacks.

- In mild cases: simple analgesics (paracetamol/aspirin) or NSAIDs (ibuprofen/naproxen) or their combination and antiemetics (metoclopramide) to hasten gastric emptying.

- Moderate cases: NSAIDs/ triptans/ ergot alkaloids and antiemetics.

- Severe cases: triptans/ ergot alkaloids and antiemetics + prophylactic therapy.

Prophylactic therapy of chronic migraine attacks include beta blockers (propanolol and timolol), calcium channel blockers (verapamil and nimodipine), anti- epileptic drugs (valproate) and anti depressant medications (amitryptaline).

To know about recent updates on the underlying mechanisms of pathophysiology and treatment strategies based on research, click here.

Thats all
- Jaskunwar Singh

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