Headaches and Dizziness

Introduction[edit | edit source]

Headaches and dizziness have numerous causes and there are many different types. This page will explore some of the key types of headaches and causes of dizziness that may be encountered in clinical practice, as well as highlighting red flags and other signs / symptoms which warrant referral.

Headache Classification[edit | edit source]

Headaches are grouped into three main areas:[1]

  • Primary headaches
  • Secondary headaches
  • Neuropathies, facial pain and other headaches

Primary Headache[edit | edit source]

Primary headaches are the most common headache type.[2] These headaches, which include migraines, tension headaches, trigeminal autonomic cephalgias, and other primary headache disorders.[3][1] They are not caused by other anatomical or physiological abnormalities. Nor are they related to inflammation or infections.[2]

Migraine[edit | edit source]

Migraine is a recurrent headache disorder which affects around fifteen percent of the population aged 22-55 years.[4] It generally begins in childhood to early adulthood although it can start later in life for some perimenopausal / menopausal women.[3] It is estimated that ten percent of children experience migraines.[5] It affects women more than men.[4] As it tends to run in families, it is considered a genetic disorder.[4] It has significant personal and economic effects[1] and is listed as the sixth most prevalent out of 328 diseases and injuries assessed in the Global Burden of Disease Study from 2016.[6]

Migraines are characterised as recurrent episodes of headaches associated with visual or sensory symptoms.[3] In some cases of migraine, a headache will occur with no warning signs and resolve with sleep.[4] However, sometimes prior to migraine, patients will experience a prodromal phase, with symptoms such as fatigue, euphoria, depression, irritability, food cravings, constipation, neck stiffness, increased yawning, and / or abnormal sensitivity to light, sound, and smell.[4] Migraines can also present with transient hemiplegic episodes. These cases require further medical investigation.[3]

Migraine headaches are usually unilateral, have a pulsating quality and are aggravated by activity. They last from a few hours up to a few days.[4] Migraines in children are generally bilateral frontal temporal headaches. It has been considered a red flag symptom if they occur in the occipital region,[3] but this has been disputed in some recent research.[7]

Migraines can occur with or without aura.

  • Migraine without aura: will generally last from four to 72 hours. Typically, pain is unilateral and of a moderate to severe pulsing type and it is aggravated by physical activity. Nausea, vomiting, photophobia, and phonophobia often accompany it[1][3]
  • Migraine with an aura: an aura refers to a sensory or neurological symptom that occurs before the migraine starts. It is usually visual - typically some type of a zigzagging crescent shape formation that occurs in the visual field,[3] but it can also refer to sensory and / or speech or language symptoms. There is no motor weakness and it develops gradually. Each symptom typically lasts no longer than an hour[1]

Tension Type Headaches[edit | edit source]

Tension type headaches (TTH) are the most prevalent of primary headaches in the general population.[8] There are four types of TTH:[1]

  • Infrequent
  • Frequent
  • Chronic
  • Probable

Lifetime prevalence rates range from 30 to 78 percent.[1] TTH are ranked as the third most prevalent condition in the Global Burden of Disease Study of 2016[6] and are more common in women.[3]

TTH are classified as recurrent episodes of headaches. The headaches may last a few minutes or continue for weeks.[9] They usually consist of a pressing or tightening pain, that is non-throbbing in nature, of mild to moderate intensity that originate in the temporal region.[3][9] They are bilateral and do not get worse with activity. While nausea and vomiting are usually absent, photophobia and phonophobia can occur.[9] They are usually accompanied by excessive tone of the suboccipital or neck muscles. Manual therapy is usually an effective intervention for this type of headache.[3]

While TTH have previously been associated with stress or psychogenic causes, there are numerous studies that suggest a neurobiological basis.[9][1]

Trigeminal autonomic cephalalgias[edit | edit source]

Trigeminal autonomic cephalalgia (TAC) is a primary headache that occurs with pain in the trigeminal distribution unilaterally in the head. It occurs with cranial parasympathetic autonomic symptoms (such as eye watering, droopy eyelids or ptosis, nasal congestion) - these features are lateralised and ipsilateral to the headache.[1][3] They are typically of short duration.

There are five different types of TACs:[1]

  • Cluster headaches
  • Paroxysmal hemicranias
  • Short-lasting Unilateral Neuralgiform Headache Attacks (either with conjunctival injection and tearing (SUNCT) or cranial autonomic symptoms (SUNA))
  • Hemicrania continua
  • Probable TAC

While the cluster headache is more common, the other three types of trigeminal autonomic cephalgia are fairly rare.[3]

Cluster headaches are recurrent and are characterised by severe unilateral pain, which has ipsilateral autonomic symptoms and often also causes restlessness and / or agitation.[10][11] Due to the severity of the pain, they can have a major impact on a patient’s quality of life.[11] The pain is located behind the eye and autonomic symptoms can include eye watering and nasal congestion.[3] Cluster headaches can last from 15 minutes to three hours and they occur in clusters. The clusters can last from weeks to months or sometimes over a year.[3]

Their cause is unknown, but it is thought to involve a coordinated, abnormal activity in the hypothalamus, the trigeminovascular system and the autonomic nervous system. It appears that the hypothalamus has a major part in generating the state that initiates an episode. The attacks themselves likely also require involvement of the peripheral nervous system.[11]

Risk factors for cluster headaches include:[3]

  • A history of exposure to tobacco smoke
  • A family history of the condition

They can be triggered by alcohol and nitro-glycerine.[3]

New Daily Persistent Headache[edit | edit source]

New daily persistent headache occurs in patients who have no previous history of headache.[1] In order to be classified as a new daily persistent headache, it must occur daily for more than three months. This headache generally has a lateral, cramping pressure quality, and is associated with photophobia, phonophobia and nausea. It is not aggravated by activity.[3] It usually has a rapid onset from a specific time - this rapid onset has to be recalled by the patient if it is to be considered / classified as a new daily persistent headache.[1] This pathogenesis of this condition is not well understood. It may be due to abnormal glial activation with persistent central nervous system inflammation. It may also be associated with patients who have a history of cervical hypermobility.[12]

Secondary Headache[edit | edit source]

Secondary headaches are headaches that can be related to an underlying medical condition or process, as well as trauma to the head or neck, infection or other disorders.[13][1] There are many different types of secondary headaches, including primary exercise headache, occipital headache versus occipital neuralgia, sleep apnoea headaches, external compression headaches, idiopathic carotidynia headache, new daily persistent headache, post-traumatic headache, medication overuse headache, trauma to the head and neck type headache, infections that cause headaches, substance abuse or substance withdrawal type headache and concussion.[1]

Primary Exercise Headache[edit | edit source]

Primary exercise headache is a type of headache with no intracranial pathology that occurs during or after exercise or exertional activity, such as a valsalva or strain manoeuvre.[14][3] Prevalence of PEH varies across studies, but it is relatively rare compared to other headaches.[14]

It can occur in hot weather or at altitude and exercise is usually sustained, strenuous, and focused on endurance.[3]

The headache is generally bilateral, pulsating or throbbing without nausea or vomiting.[14] Due to its throbbing nature, PEH symptoms can appear similar to subarachnoid haemorrhage symptoms (see below).[3] It lasts anywhere from five minutes to 48 hours.[14] There is no specific cause or disorder to produce it,[3] but it has been proposed that dysregulated cerebrovasculature may be involved.[14] It usually resolves when the specific exertion stops or is avoided.[3]

Occipital Headache / Occipital Neuralgia[edit | edit source]

Current research is still unable to distinguish the cause of occipital headaches.[15] They can be a feature of migraine headaches and TTH. However, they are thought to be initiated by tension in the shoulder, neck and scalp region that insert in the occipital region. Similarly, they may be due to compression, inflammation or irritation of the C2 sensory nerve roots[15] or due to dysfunction of the craniovertebral joints or upper cervical zygapophyseal joints.[3]

Occipital neuralgia is usually due to trauma or irritation of the nervi occipitales.[16] It causes a paroxysmal shooting or stabbing pain in the distribution of the greater or lesser occipital nerves or the third occipital nerve.[3]  Tenderness and sensory changes in the distribution of the nerve can occur. If cervical destruction alters an occipital headache, the headache may be due to a cervical structure issue.[3]

Sleep Apnoea Headache[edit | edit source]

Morning headache (i.e. occurring within 30 minutes of waking) has been associated with sleep apnoea.[3][17] However, it is important to remember that morning headaches can have two other causes:[3]

  1. Possibility of a tumour
  2. Hypertension - if blood pressure is over 160/100

Sleep apnoea headaches are classified based on the following criteria:[17]

  • Morning headache
  • Usually bilateral
  • Duration of less than 4 hours
  • Caused by sleep apnoea but no time restriction is given for improvement of headache following treatment of sleep apnoea

It is not yet clear if the headaches are due to hypoxia (reduced oxygen levels), hypercapnia (increased carbon dioxide levels) or sleep apnoea severity.[3][17]

External Compression[edit | edit source]

Another type of secondary headache is external compression. This type of headache has not been studied extensively,[18] but it is related to the ongoing stimulation of the cutaneous nerves due to pressure over the forehead or scalp[18] - e.g. due to wearing tight goggles, face masks, helmets, sweatbands, tight hats for a prolonged period of time.[3] The pain tends to be constant and worse in the area where the pressure is applied.[18] It may involve the supraorbital nerve, and can progress to become a migraine if the stimulus is maintainedI. It usually resolves when the pressure is removed.[18][3]

Carotidynia Type Headache[edit | edit source]

Carotidynia type headache occurs unilaterally in the frontal temporal facial or orbital regions. It can be subtle and gradual or instantaneous and, like primary exercise headaches, it can present like a subarachnoid haemorrhage. It is described as a constant aching, throbbing or sharp.[3]

Carotidynia is described as a tenderness over the carotid bifurcation in the neck without any specific abnormality to that artery. It has been found that this condition may be associated with a distinct thickening of the wall of the artery in that region. However, this thickening does not have an impact on the blood flow and it is speculated that it might be related to inflammation.[3] It tends to be considered an idiopathic, benign self-limiting condition.[19]

Post-Traumatic Headache[edit | edit source]

Other types of secondary headaches are due to trauma - such as subdural haematoma, epidural haematoma, intracranial or intracerebral hematoma, aneurysm, subarachnoid hemorrhage or cerebral contusion.[3]

If a patient reports that she / he is experiencing the worst headache of his or her life, this is a sign of a serious vascular event. This patient will need to seek medical care urgently.[3]

Headaches Related to Head and Neck Trauma[edit | edit source]

Headaches related to head and neck trauma are some of the most common secondary headaches. They tend to resemble migraines or tension type headaches.[1] Thus, diagnosis is made based on the relationship between headache onset and head / neck trauma. Headache must be reported to have developed:[1]

  • Within 7 days following trauma or injury
  • Or within 7 days after regaining consciousness
  • And / or within 7 days after recovering the ability to sense and report pain

Concussion[edit | edit source]

Concussion does not generally cause severe neurological deficit. However, when there is a loss of consciousness associated with concussion, this means that there has been a temporary lack of activity in the brainstem, and headaches can occur in relation to concussion.[3]

Headache may occur in conjunction with other symptoms following trauma, such as dizziness, fatigue, reduced ability to concentrate, slowed psychomotor ability, memory problems, insomnia, anxiety, irritability and personality changes. If several of these features occur post injury, the patient may be diagnosed with post-concussion syndrome.[3]

Medication Overuse Headache[edit | edit source]

Overuse of medication can also cause headache. This type of headache is classified as occurring 15 or more days per month. Patients have a pre-existing primary headache, but develop a new headache, or worsening of their existing headache as a result of regular overuse of medication (on 10 or more or 15 or more days/month, depending on the medication) for more than 3 months. This headache usually resolves when the medication is stopped.[1][3]

Headache Related to Substance Abuse[edit | edit source]

Headaches can also be related to substance abuse, such as alcohol, drug abuse, exposure to toxic substances, medication overviews, or it can be related to substance withdrawal coming down off of drugs or coming down off of alcohol.[3]

References[edit | edit source]

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 International Headache Society. International Classification of Headache Disorders (ICHD-3). Available from https://ichd-3.org/classification-outline/ (accessed 7 September 2020).
  2. ↑ 2.0 2.1 Manzoni GC, Stovner LJ. Epidemiology of headache. Handb Clin Neurol. 2010;97:3-22. 
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25 3.26 3.27 3.28 3.29 3.30 3.31 3.32 3.33 3.34 3.35 3.36 3.37 Dent D. Headaches and Dizziness Course. Physioplus. 2020.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Burstein R, Noseda R, Borsook D. Migraine: multiple processes, complex pathophysiology. J Neurosci. 2015;35(17):6619-6629.
  5. ↑ Rao R, Hershey AD. An update on acute and preventive treatments for migraine in children and adolescents. Expert Review of Neurotherapeutics. 2020. Published online.
  6. ↑ 6.0 6.1 GBD 2016 Headache Collaborators. Global, regional, and national burden of migraine and tension-type headache, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018;17(11):954-976.
  7. ↑ Genizi J, Khourieh-Matar A, Assaf N, Chistyakov I, Srugo I. Occipital Headaches in Children: Are They a Red Flag?. J Child Neurol. 2017;32(11):942-946.
  8. ↑ Jensen RH. Tension-Type Headache - The Normal and Most Prevalent Headache. Headache. 2018;58(2):339-345.
  9. ↑ 9.0 9.1 9.2 9.3 Chowdhury D. Tension type headache. Ann Indian Acad Neurol. 2012;15(Suppl 1):S83-S88.
  10. ↑ Russell MB. Epidemiology and genetics of cluster headache. Lancet Neurol. 2004;3(5):279-283.
  11. ↑ 11.0 11.1 11.2 Hoffmann J, May A. Diagnosis, pathophysiology, and management of cluster headache. Lancet Neurol. 2018;17(1):75-83.
  12. ↑ Rozen TD. New daily persistent headache: an update. Curr Pain Headache Rep. 2014;18(7):431.
  13. ↑ McGeeney B. Secondary headache: concepts and examples. Techniques in Regional Anesthesia and Pain Management. 2009; 13: 58-64.
  14. ↑ 14.0 14.1 14.2 14.3 14.4 Upadhyaya P, Nandyala A, Ailani J. Primary Exercise Headache. Curr Neurol Neurosci Rep. 2020;20(5):9.
  15. ↑ 15.0 15.1 Noseda R, Melo-Carrillo A, Nir RR, Strassman AM, Burstein R. Non-Trigeminal Nociceptive Innervation of the Posterior Dura: Implications to Occipital Headache. Journal of Neuroscience. 2019; 39(10): 1867-1880;
  16. ↑ Vanelderen P, Lataster A, Levy R, Mekhail N, Van Kleef M. and Van Zundert J. 8. Occipital Neuralgia. Pain Practice. 2010; 10: 137-144.
  17. ↑ 17.0 17.1 17.2 Suzuki K, Miyamoto M, Miyamoto T, et al. Sleep apnoea headache in obstructive sleep apnoea syndrome patients presenting with morning headache: comparison of the ICHD-2 and ICHD-3 beta criteria. J Headache Pain. 2015;16:56.
  18. ↑ 18.0 18.1 18.2 18.3 Krymchantowski, A.V. Headaches Due to External Compression. Curr Pain Headache Rep. 2010; 14, 321–324.
  19. ↑ Sempere Campello G, Arias Medina A, De Miguel P, Pilar D, Elena A et al. Carotidynia Syndrome. How to see it? Available from https://epos.myesr.org/poster/esr/ecr2015/C-2392 (accessed 7 September 2020).
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