The 'Headache' Classification of the International Headache Society (HIS) (1988) has been a major landmark document. It has helped to develop a common language for understanding headaches and to unify research in this field. It is useful in most situations but because it is complex and cumbersome, it is underutilised in practice. This article analyses the contributions, the limitations and outlines the proposed changes in the revised classification to be launched in 2003. It is hoped that more neurologists would start using this in their routine practice.

Inspite of the fact that headache is one of the most common medical complaints, most headaches in practice continue to be underdiagnosed and undertreated. Probably because most of the recent advances in headache are written in rare speciality journals. Even today many treating physicians feel that nothing much can be done for headache patients! And, since more than 90% of headaches seen in practice are primary headaches, it is to be realised that matters have come a long way in the last decade and these is now enough evidence to prove that primary headaches are a genuine potentially treatable biological problem. It is therefore important that clinicians do not err in making the right diagnosis and choosing the correct drug options. This article discusses some of the traps which may result in the sub-optimal management of primary headaches and suggests measures to avoid these 'Pitfalls'.

The biologic basis of migraine had remained unclear until about 15 years, but current migraine research has made some major advances to explain its mechanism. Migraine is currently conceived to originate in the brain. The trigger of an attack starts a depolarising event very similar to "spreading depression" of Leao in a brain that is already hyperexcitable. Hyperexcitability of cell membrane is perhaps genetically determined. Cortical depolarising events drive the trigeminovascular system through mechanisms that are largely hypothetical but might include a migraine generating centre in the brainstem to produce changes in the vessels of the cranium and meninges. Pain sensations carrying impulses are relayed back, first reaching the trigeminal ganglion caudalis and the trigeminal cervical complex in upper cervical cord from where they are relayed further up through various transmitting pathways to the brainstem, thalamus and the cortex where pain is finally perceived and registered.

Although secondary causes for headache are discemible in only about 15% of persons attending emergency departments with headache, any person presenting with acute headache needs to be investigated to rule our secondary headache disorders. The clinical approach to the patient with the worst ever headache and the features of some of the headache disorders manifesting with acute headache are discussed. Most patients with secondary headache disorders have suggestive clinical features which should not be overlooked. Appropriate use of neuroimaging, CSF analysis and angiography are essential to ascertain the underlying etiology.

Headaches are common in children. The presentation of headache in children is varied and hence the characterization of headache is more challenging. This situation is worsened further by inadequacies in the history and the effect of maturational factors. Relevant epidemiological and limitations in the applicability of International Headache Society criteria in childhood headache and the rationale for newer criteria are discussed. Migraine and tension-type headache are the common primary headache seen in children. Although there is a paucity of clinical trials the management of childhood migraine, the important role of correct pharmacological approach has been delineated. The pivotal role of non-pharmacological treatment is emphasized.

The Classic presenting features of both migraine with and without aura have been clearly defined. Occasionally however migrainous headaches are accompanied by abrupt appearance of focal and ominous neurological signs. Such attacks can be labelled as migraine variants and the diagnosis in reality is one made by exclusion of other CNS diseases. Some but not all such conditions are mentioned in the International Headache Society (IHS) classification under the general heading of migraine with aura. Rarely, the focal neurological deficit may outlast the migraine attack by days and occasionally with appearance of structural brain lesions on neuroimaging. Such attacks have been labelled as complicated Migraine by the IHS. The present review deal with the clinical, radiologic and pathophysiologic aspects of both these conditions - migraine variants and complicated migraine.

Rare though it may be, cluster headache needs to be correctly diagnosed and specifically treated because it is the most painful of all primary headaches. An important reason why cluster headache and other recently described short-lasting headache syndromes that are now grouped together as trigeminal-autonomic cephalgias (TACs) continue to be suboptimally managed is because they often go unrecognised or are wrongly diagnosed as migraine. This article discusses the salient clinical features of cluster headache, the recent hypotheses regarding its pathophysiology, and the treatment options available to control it.

Chronic daily headache (CDH) still remains a relatively unexplored entity in our country. Misconceptions are common, unnecessary investigations are done often and inappropriate therapy is prescribed. Analgesic overuse in seldom recognized. The present report is a detailed analysis of CDH in an Indian setting. CDH has been defined as headaches occurring more than 15 days per month for more than 3 months (secondary causes excluded). Over two years (1998-99) 876 cases (51.2% of all primary headaches) were seen. More than one year follow up data ware available in 232 subjects (m-52; F-180). The distribution of these cases were as follows: a) Chronic tension type headache (CTH) : 24(10.3%); (b) transformed migraine (TM) : 166(17.6%); (c) migraine-CTH-from episodic tension headache : 12 (5.2%); (d) new persistent CDH : 3 (1.3%); and (e) chronic post-traumatic headache : 27 (11.6%). There were 166 cases of TM (M:F-1:4.7; age 26-58 yrs.). History of past episodic migraine was present in all. Transformation had been gradual (89.2%) or acute (10.8%). Possible factors in transformation included - psychological stress (43.8%), analgesic overuse (20.9%), ergot overuse (4.2%). Hormone replacement therapy seemed to be implicated in 3 female subjects. Analgesic overuse was limited between intake of 600-2400 mg of aspirin equivalent per day (mean 735 mg). Ergot overuse varied between 1-3 mg/day of ergotamine for 3 or more days per week. With medical therapy approximately 70% TM and 40% CTH patients noted significant improvement. About 80% of these relapsed on therapy withdrawal. CDH in India is not uncommon. Analgesic/ergot overuse needs to be recognized early. The average dose of analgesic implicated in CDH seems much less compared to that reported from the West.

Some headaches are relatively uncommon. They may be either primary of secondary and their recognition is dependent on the characterization of symptoms as well as identification of certain specific situations in which they need to be considered in the differential diagnosis. Primary headache syndromes like the paroxysmal hemicranias, SUNCT (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing), cough headaches and hypnic headaches are uncommonly encountered in routine clinical practice. They have subtle unique features and specific therapies which differentiate them from the commoner primary headaches. Among the secondary causes, headaches may be an uncommon presenting feature of known clinical disorders, lack of awareness of which may result in significant morbidity. These disorders which may present with headache as the main symptom will be the focus of discussion in this review.

Assessment of patients with migraine is often confounded by the concurrent occurrence of co-morbid disorders. At times the accompanying clinical symptomatology mimics a psychiatric disorder of epilepsy. This can have profound effects on the prognosis and treatment of these patients. The term comorbidity encompasses all such concurrent disorders. This article reviews evidence based, peer reviewed literature on migraine comorbidities and attempts to clarify diagnostic issues of relevance to the clinician.

There are many reasons to suggest a link between headache and hormones. Migraine is three times common in women as compared to men after puberty, cyclic as well as non-cyclic fluctuations in sex hormone levels during the entire reproductive life span of a women are associated with changes in frequency or severity of migraine attack, abnormalities in the hypothalamus and pineal gland have been observed in cluster headache, oestrogens are useful in the treatment of menstrual migraine and the use of melatonin has been reported in various types of primary headaches. Headache associated with various endocrinological disorders may help us in a better understanding of the nociceptive mechanisms involved in headache disorders. Prospective studies using headache diaries to record the attacks of headache and menstrual cycle have clarified some of the myths associated with menstrual migraine. Although no change in the absolute levels of sex hormones have been reported, oestrogen withdrawal is the most likely trigger of the attacks. Prostaglandins, melatonin, opioid and serotonergic mechanisms may also have a role in the pathogenesis of menstrual migraine. Guidelines have been published by the IHS recently regarding the use of oral contraceptives by women with migraine and the risk of ischaemic strokes in migraineurs on hormone replacement therapy. The present review includes menstrual migraine, pregnancy and migraine, oral contraceptives and migraine, menopause and migraine as well as the hormonal changes in chronic migraine.

Pharmacotherapy for migraine involves treatment for the acute attack as well as using long-term prophylaxis in order to reduce the frequency and severity of the attacks. Based on severity, there are a number of drugs available to treat the acute attacks. For mild to moderate attacks, analgesics, NSAIDs and Ergotamine are effective but severe attacks may need Dihydroergotamine (DHE) or a triptan. Sumatriptan and the second generation triptans have revolutionized the acute treatment of migraine. Early and appropriate treatment holds the key to successful therapy of the acute attack. This article discusses the various acute treatment options available.

Preventive therapy in migraine constitutes an important aspect of migraine management especially in patients who are not controlled or have significant disability despite taking drugs for acute management. In spite of te recent advances in understanding of the pathophysiology of migraine, the mechanisms of action of many preventive drugs are largely unknown. Further, these provide only about 50% reduction in frequency in about 2/3rds of migraine sufferers. Hence, risk-benefit ratio must be considered while prescribing these agents. Recent efforts to undertake large-scale meta-analysis to assess the efficacy of these agents have been rewarding and consensus guidelines have evolved. Propanolol, metoprolol, amitriptyline, sodium valproate, flunarizine and lisuride have emerged as first line drugs. The role of newer anti-convulsants and botox injections in refractory cases are being investigated. Availability, co-morbidities, medical contraindications, concomitant acute therapy and costs are important determinants for choosing a particular agent. This article reviews the guidelines to be followed in choosing the prophylactic treatment options for migraine.