Headaches are a common reason for visiting a Neurologist, a primary health care provider or an emergency department in a hospital. Most headaches that cause a medical visit are benign in nature in that the pain is self limited and mortality and or irreversible morbidity is unlikely. These benign headaches may be one of primary headache disorders such as migraine or tension type headache, cluster headache or secondary cause of headache such as viral sinusitis or cervicogenic headache (1). For most patients management should consist of identifying the headache disorder and providing patients with a specific diagnosis identifying causative or contributing factors as this assists the clinician in making the correct diagnosis and apply the most appropriate treatment leading to a favourable outcome for the patient. At times, headaches are symptomatic of an underlying process that requires prompt diagnosis and urgent medical treatment to reduce threats to life or limb. Suspicion of these disorders mandates emergent diagnostic testing to exclude the disease (1).



The diagnosis of headache can be challenging as it shares many properties similar to migraine. According to the International Headache Society (IHS) they have listed a classification of headaches- the International  Classification of Headache Disorders (ICHD-II), they state that a migraine is predominantly a unilateral severe form of a headache that infrequently shifts sides. Headaches share similar properties to migraines so initially a diagnosis between the two can be challenging (2).

At this point, it is important to illustrate to clinicians some of the possible differential diagnosis “red flags” of headaches which with careful history taking can alert them to the following signs and symptoms (1):
i) First, worse or sudden onset, whereby the clinician should be aware of an abrupt onset, worse headache ever, no previous history which could indicate aneurismal subarachnoid heamorrhage, cervical artery dissection, other forms of intracranial haemorrhage.
ii) Progressive headache, raises concern for space occupying lesion, neoplasms-metastatic or benign or malignant.iii) Headache associated with focal signs and symptoms, need to exclude mass lesions, ischaemic or haemorrhagic stroke, vascular pathology, or infection.
iii) Headache associated with fever and stiff neck, such as meningitis, encephalitis.
iv) New onset headache after 55 years of age, artherosclerotic diseases as well as temporal arteritis.
v) Post-traumatic haematoma, as a result of blunt trauma or other forms of head trauma, blood may collect in the brain parenchyma, subarachnoid space, subdural space, or epidural space.
vi) Pituitary apoplexy, a haemorrhagic infarct of the pituitary may cause devastating presentation of a headache, bi-temporal visual field deficits, opthalmoplegia and cardiovascular collapse.
vii) Hypertensive headache, the International Headache Society defines a hypertensive headache as one in which there is a paroxysmal increase in systolic or diastolic blood pressure to greater than 160 mm HG or 120mm Hg respectively. The headache must be either bilateral or pulsating or precipitated by physical activity. It must develop during the hypertensive period and resolve within 1 hour after normalisation of blood pressure.

Subsequently making a diagnosis of headache depends on the history given by the patient, key features including; length of the pain / frequency of episodes / duration of episodes / principal site and radiation quality of the pain / onset / associated features, what precipitates the pain, what relieves the pain (3). The International Classification of Headache Disorders (ICHD-II) are (4):
(i) Primary headaches: Migraine; tension-type headache; cluster headache and other trigeminal autonomic cephalgias; other primary headaches.
(ii) Secondary headaches: Headache attributed to head or neck trauma; headache attributed cranial or vascular headache; headache attributed to non-vascular intracranial disorder; headache attributed to substance or its withdrawal; headache attributed to infection; headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures; headache attributed to psychiatric disorders.
(iii) Cranial Neuralgias Central and Primary Facial Pain and Other Headaches: Cranial neuralgias and central causes of facial pain; other headache, cranial neuralgia, central or primary facial pain.

Discussed will be some of the different types of headaches which can present to the clinician, the mechanisms involved, hence the diagnosis. As merely identifying all the different types of headaches and treatment options does not aid in good clinical reasoning / rationale, so additional information to the clinician in making a diagnosis are (3):
i) Factors such as the frequency and duration which can be grouped together as the temporal pattern of the pain: Thunderclap headaches, having characteristics of subarachnoid hemorrhages or a precursor response to benign sex headaches; migraine; chronic daily headache; chronic daily headache plus migraine; cluster headache; intracranial lesion; post-traumatic headache such as whiplash injury.
(ii) Site of headaches: Ice cream headache-typically frontal and midline, can be at site of habitual migraine, possibly due to the distribution of the trigeminal pathway; sinusitis-usually around the ethmoidal, sphenoidal and frontal sinuses; migraine is unilateral in 2/3 of sufferers, pain is commonly referred to the occipital area, conversely occipital pain maybe referred to the front; cluster headache is always around the eye, radiating down over the face or the back of the head, described as tense and boring; tension headache is usually bilateral and variously described as feeling like a weight on the head;  trigeminal neuralgia has the characteristic of sudden, stabbing pain usually with the second or third divisions of the trigeminal nerve-maxillary, mandibular.

Key types of headaches:
Central sensitization, there is a clear link with headache and central sensitization. As this can affect treatment whereby peripheral inputs may no longer be effective, as the pain is maintained centrally. These changes can have a genetic link, as there have been studies to show the appearance of early response gene products, such as c-fos. These early response gene products may play a role in neuronal wind-up enhanced responses of neurons to stimuli and may be an early part of the response of central sensitization. The clinical correlate is the development of cutaneous allodynia, with normally non painful stimuli becoming painful e.g touching the scalp and brushing the hair (5).

Tension-type headaches (TTH) have symptoms described as episodic or chronic, those described as episodic are described as pressing, tight, mild-moderate, bilateral and not worsened by exertion, as compared to migraine which is worsened by exertion / physical exercise (5). Chronic classification is if they occur more than 15 days per month. Associated features include stress, anxiety, depression, analgesic overuse or muscle contraction. Muscle contraction may be due to poor posture, or temperomandibular joint dysfunction. Psychological features may include aggression, hostility or resentment, physiologically these patients seem to have low pain thresholds (3).
Cervicogenic headache (CeH) is a secondary headache arising from a disorder or lesion within the cervical spine or soft tissues of the neck. The reported prevalence of CeH varies from 0.4% to 15% of the headache population in different epidemiological studies. Since the pathogenesis of TTH and CeH is considered to be heterogeneous, different therapeutic approaches might be needed. As the genesis of CeH involves pain referred to the head originating from joint structures in the upper cervical spine (6).
CeH perceived in the forehead or orbital region requires convergence between trigeminal and cervical afferents, whereas cervicogenic headache perceived in the occiput requires convergence between certain cervical and other cervical afferents. The overlap between terminals of the trigeminal nerve and those of the upper three cervical nerves provides the substrate for the possible sources of cervicogenic headache (7). Associated symptoms of CeH may include nausea, vomiting, dizziness, phono-photophobia occasionally dysphagia or ipsilateral blurred vision. The clinical presentation provides significant overlap with migraines suggesting that their pathogenesis may in somewhat be related. One noteworthy difference between CeH and migraine pain is that migraine pain classically begins in the occulofrontotemporal region. However 12% of migraines without aura may start in the neck or occiput and up to 64% of migraine sufferers experience neck pain before during and after an attack, CeH can also co-exist with migraine (2).

Medication-Overuse Headache (MOH) is a controversial medical condition that according to recent epidemiological trials is the 3rd most frequent headache type after migraine and tension-type headache (TTH) (7).  The current ICHD-II version describes MOH as a headache presenting on or over 15 days per month after regular use of triptans, ergotamines, opiods, or analgesics for over 3 months with newly developed or markedly worsened headache during medication overuse. How the pathophysiological mechanisms of MOH works are not entirely clear. A number of factors have been discovered to play an important role in the development of this disease such as genetic background, peripheral and central receptor regulation, specific psychotropic effects and behavioural conditioning (8).  Regular exposure to a substance will induce substantial changes in expression and sensitisation of receptors as well as changes for the threshold of receptor activation. The extent of these changes and the speed in which these changes occur depend on the receptor type and the duration and concentration of drug exposure (9). It has been shown that chronic or frequent exposure to serotonin (5-HT) agonists may lead to down regulation of 5-HT receptors and change central inhibitory pathways in human beings. Aspirin reduces 5-HT receptor binding capacity in the short term, as well, aspirin inhibits cox I and cox II enzymes which are for prostoglandin synthesis (10). Paradoxically the effect of aspirin on prostoglandin synthesis is that prostoglandin relieves dorsal horn nociceptive neurons from the inhibitory control by glycinergic neurons. Therefore prostoglandin induced headache is caused by activation and sensitisation of meningeal nociceptors (11).
Thus the down regulation of 5-HT receptors or prostoglandin synthesizing enzymes in anatomical structures that are involved in the transmission or modulation of nociceptive signals, such as the periaqueductal grey matter (which has serotonergic descending inhibitory pathways mainly to trigeminal nuclei ) may lead to the impairment of anti-nociceptive activity and subsequently result in a permanent feeling of head pain (9).

Clinical management of headaches:
In determining the treatment options, relating to the ICHD-II classification, this can lead the clinician to a diagnosis, hence for such headaches such as CeH and TTH, treatment options include spinal manipulative therapy, indomethacin, counselling, relaxation, trycyclic antidepressants, non-steroidal anti-inflammatories, benzodiazepines and acupuncture (6). MOH, once identified immediate drug withdrawal should begin (8). Cervical spine nerve blocks to the upper 3 cervical nerves can also be used (7). Psychosocial factors can be considered and referral to an appropriate Multidisciplinary Team (MDT) member can also be beneficial (12). This can be shown in determining a pain formulation, as it is important to identify factors such as fear-avoidance beliefs, catastrophising or low confidence in functioning when in pain e.g. signs of anxiety can cause prolonged muscle spasm, vasoconstriction, ischemia and release of pain producing substances. An example of a MDT member such as a Clinical Psychologist using Cognitive Behavioural Therapy (CBT) to help deal with low confidence, feelings of depression and catastrophising beliefs. This form of management can also be considered for cases where central sensitization may be occurring (13).

1) Freidman, B.J. & Lipton, R.B. (2012). Headache Emergencies: Diagnosis and Management. (pp. 43-45).

2) Hoskin, W.T., Pollard, H.P. & Tuchin, P. (2006). The Neurogenic Pathogenesis of Migraine: A
Commentary. (pp. 69-70).

3) Lance, J. (2009). Clinical Aspects of Neurobiology PAIN5010. Module 4: Headaches. University of

4) International Headache Society -ICHD-II. (2005). 25. (pp.460-465).5) Ward, T.N. & Levin m. (2004). Diagnosis and pathophysiology of migraine. (pp. 385-387).

6)  Fernandez-des-las-Penas, C. et al. (2005). Spinal manipulative Therapy in the Management of
Cervicogenic Headache. (pp. 1260-1262).

7) Bogduk, N. (2001). Cervicogenic headache: Anatomic Basis and Pathophysiologic Mechanisms. (pp. 381-

8) Obermann, M. & Katsarava, Z. (2007). Management of medication-overuse headache. (pp. 1145-

9) Diener, H. & Limmroth, V. (2004). Medication-overuse headache: a worldwide problem. (pp. 475-483).

10) Siddall, P. (2012). Headache. PAIN5010 Clinical Aspects of Neurobiology, Online discussions.

11) Wienecke, T & Olesen, J. et.al. (2009). Prostoglandin induces headache in healthy subjects. (pp. 509-

12) Craig, K.D. (1999). Emotions and Psychobiology. In P.D. Wall and R. Melzack. Textbook of Pain.
(pp. 339).

13) Linton, S.J. & Nicholas, M.K. (2008). After assessment, then what? Integrating findings for successful
case formulation and treatment tailoring. (pp. 95-102)

Spinal Care provide professional support and guidance for a wide range of conditions which includes headache pain management, and can identify the best solution as well as the best techniques to assist in further prevention of them in future, so that you can have a happier, pain-free life