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the severe headache emergency – part 3

The severe headache emergency – part 3

The patient we are attending is complaining of a severe headache and photophobia. She does not have fever or signs of meningism. The two major threats of subarachnoid haemorrhage and meningitis are possible causes but not stand out for suspicion. However the patient has confirmed a long history of suffering migraines. She has a number of them every year with them sometimes lasting for more than a day. This presentation is pretty much the same as on other occasions. She normally manages her migraine herself.

Treatment of migraine can be divided into two streams. One part aims to preventing the number of and duration of episodes in the first place. The other part combats those that do occur. Both are commonly employed by migraineurs. Options for managing acute episodes can be further divided into two groups. Those that provide non specific therapy such as paracetamol, aspirin and non steroidal anti-inflammatory drugs. These are better suited for mild to moderate pain. Opioids can also be considered non specific analgesia. Therapies more specifically tailored to migraine are better for more severe or unrelieved pain. The triptans are first line examples of this therapy. Therapies that intend to prevent migraine episodes in the first place include some of the beta blockers, calcium channel blockers, antidepressants and antiepileptic medications.19

Despite aspirin being a reasonable first option for a clearly diagnosed headache, it is not suitable for prehospital responders. One possible headache cause to be excluded is intracranial haemorrhage, so antiplatelet aspirin may offer more problems than solutions.

Triptan drugs help migraine by binding to serotonin receptors. They work best if taken early in the onset. A disadvantage of tryptans is that they can cause vasoconstriction making them less suitable where there is severe cardiovascular disease or hypertension present. They also don’t combine well with serotonin reuptake inhibitors with risk of excessive serotonin.19

The trigeminal nerve (the fifth cranial) plays the major role in sensation and motor actions of the face and jaw. This nerve gets a major mention when any head pain is noted since the sensory role includes touch, temperature and pain. It is called the trigeminal nerve as it branches into three parts; the ophthalmic, maxillary and the mandibular nerve.

Nerve messages are passed on by neurotransmitting chemicals with two of the most common being dopamine and serotonin. The neurotransmitter is the chemical, the receptor is what they bind with that switches on some message transmission. A neurotransmitter agonist mimics the action of the neurotransmitter. Dopamine agonists for example are used for treating Parkinson’s. Antagonists block or interfere with the action of the neurotransmitter. This is an important point to keep in mind since two dopamine agonists in common prehospital use are prochlorperazine and metoclopramide.

An earlier theory for migraine cause was that it involved cerebral vasodilation within the brain. By blocking the dopamine action, the vascular response could be eased. This theory has largely been at least partly replaced.

The brain itself does not have pain receptors. Instead the trigeminal nerve provides for this input from structures within and around the brain including muscles, blood vessels and other nerves. Sensory receptors in the meningeal blood vessels communicate with the trigeminal nerve. With migraineurs this process is exaggerated. Inflammation, vasodilation and unhelpful cellular responses all produce and enhance the sensation of pain irrespective of the amount of vasodilation.

To help manage this response, the triptan drugs seek to antagonise the serotonin activities whilst dopamine agonists can be used concurrently to address this other major neurotransmitter.

The antiemetics prochlorperazine and metoclopramide are commonly employed in prehospital use. There is a body of evidence and support for use of both for migraines. Arguably prochlorperazine is the most effective however metoclopramide is a reasonable alternative.10 Alternatively inhalation analgesia such as methoxyflurane may not go any way to treating the cause of the pain but may still be effective in providing some interim analgesic relief.

With migraine, the headache is arguably the strongest clue. Though there are various migraine presentations the headache is most commonly severe, frequently throbbing or pulsating and in the majority of cases one sided. It can be made worse by movement and exercise. Occasionally it is both sides or frontal but not usually at the back of the head. It can last for hours to days. Migraine is typically divided into with or without an aura. What is of great concern when migraine is suspected is the finding of meningism, fever or changes in consciousness.20

The aura with migraine is an interesting symptom. This can accompany other neurological problems including seizures. An aura is best described as a change in what the patient perceives. It can involve senses, commonly visual or smell. Alternatively it can involve confusion and changes in behaviour. Whilst none of these are particularly problematic, they can help to assess that this problem is indeed consistent with previous episodes.

Aura with migraine does cause some concern for the patient in the longer term. Migraine with aura affects about one in three migraineurs with visual symptoms common.9 There is some recognised association between this type of migraine and the possibility of stroke in the longer term.7,8,9,13 Though unclear as to why, one theory is that the arteriosclerosis that can lead to ischemic or even intracerebral haemorrhage also causes endothelial changes, inflammation and irritation to the trigeminal nerve.1,9,11,13 This provides a direct link between migraine and stroke. However before panic sets in, it must be remembered that as many as one in five people have migraine affect their lives at some time making it likely that may people will also have stroke as well.13 Many will simply share risk factors for stroke.

There are other causes of severe headache. Cerebral vasoconstriction from non migraine causes can. Migraine has some association with cerebral vasodilation. Cerebral vasoconstriction can similarly be seen to be problematic and associated with headache. This can be caused by recreational drugs such as ecstasy and amphetamine, prescription medications particularly serotonin uptake inhibitors2 and tryptans and even some nasal decongestants such as ephedrine. Other medical causes can lead to indirect cerebral vasoconstriction. These include eclampsia, head injury, intracerebral and subarachnoid haemorrhage.

Exactly these leads to cerebral vasoconstriction is not always well understood. Likely theories include changes in and dysfunction of the endothelium from excessive sympathetic stimulation or some other mediator such as sertotonin or nitric oxide. As with migraine, the best treatment is to try to identify and avoid trigger factors. There are medication options none of which have strong evidence for support. They include steroid use and calcium channel blockers.4 Headache caused by sudden vasospasm though is more likely to produce thunderclap headache.

Cervical artery dissection, which can present similarly to artery spasm is another. Tension headache is arguably the most common form of headache but is commonly limited to moderate or less in pain severity. Causes vary and often unknown but can include stress, eyestrain or tiredness. Some causes will be idiopathic with others from trauma including to the neck.4 Importantly for prehospital responders, diagnosis will frequently not be available. Treatment will often be non specific to the cause as it will be in hospital. Erring to the most reasonable worst case scenario must be strict.

Illness, such as gastrointestinal, can lead to dehydration and the feeling of headache which is usually milder in intensity. Administration of intravenous fluid therapy to correct severe dehydration may be of benefit if the headache is thought to be from this cause.

Opioids do not have a major role or many friends when it comes to treating the patient with severe headache. They can cause dependency and do not aim to treat any underlying cause. They can also be the target of drug seeking behaviours in some cases. However there is the concept of rescue therapy where the patient with severe headache that cannot be relieved by other means is provided with opioids in desperation to seek some pain relief. This should be the perception and position for opioids. All else has failed, there is no immediate in hospital prospect of an alternative, better suited, therapy and the patient continues to have severe unrelieved pain.

Opioids may be the only helpful analgesia available for the patient with acute stroke with severe headache. Though there is some risk of causing drowsiness or hypotension, both of which could be problematic, the desire to provide some relief from the unrelenting headache severity is overwhelming. In such cases access to an emergency department should not be readily at hand. The crushing pain of subarachnoid haemorrhage may not benefit from any analgesia option. Given the severity of this pain, the early administration of opioids is usually a reasonable choice. For the migraineur though other alternatives should be given a chance to work first.

A well documented problem with headache medications is the so called rebound headache. Correctly called overuse of headache medication, this is a problem where headache severity and occurrence can actually increase directly as a result of significant use of the medication. This problem applies only to people who already have a headache problem. Taking analgesia for other problems not related to headache will not then go on to produce headaches.

Overuse rebound headaches result from significant and regular use of analgesic medications for pre-existing headaches. It does not happen in response to short term or occasional use. Medications commonly implicated include non steroidal anti-inflammatories, opioids and tryptans. Despite this problem, it should not necessarily have any influence on the acute rescue management that can be provided by prehospital responders.

Recovery from overuse rebound headaches is straight forward though difficult and not always successful. The patient ceases using the problematic medication and either modifies the way they use the drug in future or finds a suitable alternative. The difficulty comes in the rise in headache frequency observed during the withdrawal period. Withdrawal from the problematic medication may on occasion require hospitalisation. Nausea, vomiting, cardiovascular disturbance, anxiety, restlessness and sleep disturbance are commonly observed along with the increased headache. Alternative medications may not work and the patient may have a natural tendency to lapse back into using the problematic drug. The real trick is to ensure patients do not enter into this problem in the first place, particularly with drugs such as opioids.

References

1. Headache and the Risk of Stroke:  A Prospective Observational Cohort Study Among 35 056 Finnish Men and Women Pekka Jousilahti, MD, PhD; Jaakko Tuomilehto, Daiva Rastenyte, Erkki Vartiainen, Arch Intern Med. 2003;163(9):1058-1062

2. Cerebral vasoconstriction and stroke after use of serotonergic drugs A. B. Singhal, Caviness, A. F. Begleiter, E. J. Mark, G. Rordorf, W. J. Koroshetz Neurology January 8, 2002; 58(1):130-133

4. Reversible Cerebral Vasoconstriction Syndrome: An important cause of severe headache Li HueyTan, Oliver Flower Emergency Medicine International Volume 2012, Article ID 303152, 8 pages

9. Migraine and risk of haemorrhagic stroke in women: prospective cohort study Tobias Kurth, Carlos S Kase, Markus Schurks, Christophe Tzourio, Julie E Buring, BMJ 2010;341:c3659

11. Cerebral infarct presenting with thunderclap headache Bengt A. Edvardsson Æ Staffan Persson J Headache Pain (2009) 10:207–209

13. Migraine and stroke: Perspectives for stroke physicians Tobias Kurth, Hans-Christoph Diener Stroke, 2012; 43:3421-3426

19. A review of current European treatment guidelines for migraine Fabio Antonaci, Cezar Dumitrache, Ilaria De Cillis, Marta Allena. J Headache Pain (2010) 11:13–19

20. Migraine: diagnosis and pharmacologic treatment in Emergency Department. V Bounes, JA Edlow European Review for Medical and Pharmacological Sciences 2011; 15: 215-221

One thought on “the severe headache emergency – part 3

  1. Michael / Reply November 25, 2017 at 2:11 am

    You said it very well

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