Tension Headache

Re @embasic The proper dose of opioids for acute headache is 0.0 mg/kg #foamed
— Mike Abernethy (@FLTDOC1) April 3, 2014

Tension Headache and Medication Overuse headache are very similar in my head (the former sometimes literally), so I'm going to cover both of them together!

Tension Headache
Tension headache can be episodic or chronic. It is normally described as a featureless headache. It can cause daily or very frequent headaches, lasting minutes to days.
- Symptoms begin before the age of 10 years in 15% of people with chronic tension-type headache.
- It affects 4.1% of the population
- 65% of cases are women
It is thought to be triggered at least partially by stress.

The 2004 International Headache Society criteria for chronic tension-type headache are:
- Headaches on 15 or more days a month (180 days/year) for at least three months
- Pain that is bilateral, pressing, or tightening in quality and non-pulsating, of mild or moderate intensity, which does not worsen with routine physical activity such as walking or climbing stairs
- Presence of no more than one additional clinical feature (mild nausea, photophobia, or phonophobia) and without moderate/severe nausea or vomiting.
- Causes of normal headache --> chronic daily headache:

Interesting review of tension headache therapeutics in ED http://t.co/74XEv6lqMG #FOAMed #FOAM4GP
— Casey Parker (@broomedocs) March 15, 2014

Treatment
- Prevention is better than cure
- Amitriptyline or mirtazapine are both helpful
- CBT

Medication Overuse Headache
Medication overuse headache is difficult to diagnose, as the type of headache that develops varies eg patients with underlying migraine report migraine-like daily headache.
It is caused by tolerance, and withdrawal.
They normally use large quantities of medication (eg 35 doses/ week; six different drugs). Opiods and barbiturates are more likely to cause it.
It is the frequence rather than the absolute quantity that is important. Caffeine is thought to make you more susceptible.
- Prevalence around 1% of adults and 0.5% of adolescents (aged 13–18 years)
- Most prevalent in those aged around 40–50 years and affects about three times more women than men.

Symptoms improve 1- 6 months after withdrawal of medication. Simply recognising medication overuse and advising patients about its bad effects can be enough to significantly reduce the problem- in one study after identification of the problem, 76% no longer overused medication, and 42% no longer had chronic headache. The rate of relapse is high (between one-third and one-half of patients in specialist headache clinics), being more likely with opiates and simple analgesics than triptans.

References
http://dtb.bmj.com/content/48/1/2.abstract
http://learning.bmj.com/learning/module-intro/chronic-tension-headache.html?moduleId=10007571&searchTerm=%E2%80%9Ctension%E2%80%9D&page=1&locale=en_GB
http://bestpractice.bmj.com/best-practice/monograph/12.html
http://www.bmj.com/content/336/7635/88?variant=pdf&sso=
http://emupdates.com/2009/01/03/664-features-of-tension-headache-causes-of-subarachnoid-hemorrhage-what-of-the-population-has-a-berry-aneurysm-diseases-associated-with-berry-aneurysm/ http://www.bmj.com/content/340/bmj.c1305
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1517

Cluster Headaches

Cluster headaches are severe unilateral headaches. They used to be called migranous neuralgia. They are short lasting and are accompanied by autonomic symptoms. Less than 1% of patients have cluster headache, and it affects men more than women (3- 6 times more), and young people (in their 30s) rather than old people. 85% of patients smoke. They present similarly in men and women, but women tend to have more migrainous type symptoms. Alcohol, nitroglycerine, exercise, and elevated environmental temperature are recognized precipitants of acute cluster attacks.


Symptoms
- Short bouts of pain, lasting weeks or months
- Bouts may occur up to eight times a day
- Follow a circadian rhythm, with a 24hour cycle
- One sided in the orbital, supraorbital or temporal regions
- Associated with autonomic symptoms (ptosis, miosis, eye watering, bloodshot eye, runny nose, blocked nose).
- Autonomic symptoms occur on the same side as the pain

Official Diagnosis
A diagnosis of cluster headache is supported by at least five attacks that fulfil the following criteria:
Severe pain on one side in the orbital, supraorbital, or temporal region which lasts 15 to 180 minutes if left untreated.
At least one of the following on the same side:
   Bloodshot or watery eye
   Blocked or runny nose
   Eyelid oedema
   Forehead and facial sweating
   Miosis or ptosis, or both
   A sense of restlessness or agitation
Attacks that occur every other day at a frequency of up to eight per day
Other causes have been excluded.

Migraine vs Cluster Headache

 Alcohol induces cluster headache quickly, migraines some hours after.

Treatment
To manage patients with cluster headache you should treat the acute attack and consider prophylaxis against further attacks

Oxygen
- 100% via non re-breath mask for at least 20 minutes
- 60% of patients respond to oxygen therapy
- More beneficial at the onset of symptoms

Sumatriptan
- 6mg sc sumatriptan relieves pain in 20minutes in 75% of patients
- Oral triptans are too slow
- Triptans contraindicated with cardiovascular, cerebrovascular disease and untreated arterial hypertension. Do NOT use with MAOIs or ergotamines.
- Side effects include chest pain and distal paraesthesiae.

Ergotamines
Oral ergotamine has been used to treat cluster headache for more than 50 years, but there is little evidence available to support its effectiveness.

Lidocaine
Applying lidocaine nasally is effective in about one third of patients. The suggested dosage is 1 ml with a concentration of 4-10%, given on the same side as the pain. The patient should lie back with their head turned to the affected side after application. Most of these studies are small, and the effect is unlikely to be clinically beneficial.

Steroids
Up to 80% of patients with cluster headache respond to steroids. Start with 60-100 mg of prednisolone once a day for at least five days. After this you should try to decrease the dosage by 10 mg every day.

Third Line Treatment
Pizotifen, valproic acid, topiramate and capsaicin. Prevent with verapamil or lithium.

Follow Up
It is recommended that patients attending with cluster headaches should be followed up in neurology outpatients for consideration of further imaging as there is a link with pituitary adenoma.

Paroxysmal hemicrania
Paroxysmal hemicrania is rare. It is similar to cluster headaches but patients have shorter, more frequent attacks. They have a good response to indomethacin. This is one of the diagnostic criteria. Within three to seven days of starting indomethacin at an adequate dosage the attacks disappear. The usual dose is 50 mg three times per day. It is worth trying a trial of indomethacin even if the headache is not typical of paroxysmal hemicrania; if patients are going to respond, they will do so quickly.

http://www.enlightenme.org/learning-zone/doc-my-head-hurts
http://www.bmj.com/content/344/bmj.e2407
http://jnnp.bmj.com/content/70/5/613.full
http://www.pn.bmj.com/content/1/1/42.full.pdf
http://www.bmj.com/content/344/bmj.e2407.pdf%2Bhtml
http://n3.learning.bmj.com/learning/modules/flow/JIT.html?execution=e1s1&_flowId=JIT&moduleId=5004479&status=LIVE&locale=en_GB&action=start&sessionTimeoutInMin=90
http://cks.nice.org.uk/headache-cluster
http://publications.nice.org.uk/headaches-cg150
http://www.sign.ac.uk/guidelines/fulltext/107/index.html

Practical Procedures: Cardioversion and Pacing

I very much didn't like doing cardioversions, or pacing until I actually did them! I still find it difficult to remember the numbers, so I've got myself a special memory card - it's duplicated information elsewhere, but better too many times than not enough.

Syncope

Syncope is common, and difficult to investigate because by definition, the patient has recovered from the event! It is summarised here. There are five main causes to consider:

1. Neurocardiogenic or vasovagal (emotional, situational or orthostatic triggers)
2. Cardiac
3. Orthostatic
4. Neurological / psychiatric (5%). Neurological causes of syncope include basilar artery migraine, vestibular dysfunction and vertebrobasilar ischaemia. Psychiatric syncope is a recognised syndrome consisting of syncopal episodes found in anxiety, depression and conversion disorder that resolve with treatment of the psychiatric disorder.
5. Essential (no cause found -35-50%).

These will all be covered in turn, and separately. There are scoring systems used to help risk-stratify syncope (very important).  I do like EM Basic's quick approach:

Syncope + headache= subarachnoid or intracranial hemorrhage

Syncope + neuro deficit= stroke/TIA or intracranial bleed

Syncope + confusion= seizure

Syncope + chest pain= MI, PE, or aortic dissection

Syncope + back/abdominal pain in older patient= abdominal aortic aneurysm (AAA)

Syncope + positive HCG= ectopic pregnancy

Young with Syncope R/O: Structural heart prob HOCM Elect (brugada, prolonged QT, arrhythmia) Hypoglycaemia CNS insult Abnormal Lytes #FOAMed
— Meshal AlBassam (@meshal_albassam) March 16, 2014

OESIL (Osservatorio Epidemiologico della Sincope nel Lazio) Score

• age over 65 years;
• previous history of cardiovascular disease;
• syncope without prodrome and
• abnormal ECG

The score predicts 12 month mortality which rises from under 1% for patients with no risk factors to over 50% in patients with all 4 risk factors. I've never seen this used in clinical practice, or heard of it.

The San Francisco Rule
The San Francisco rule identifies high risk patients based on the presence of the following factors:

• History of congestive cardiac failure
• Haematocrit < 30%
• Abnormal ECG
• Complaint of shortness of breath
• Systolic Blood Pressure < 90 mm Hg

The presence of any factor is considered sufficient for the patient to be high risk.The rule is 98% sensitive and 56% specific to predict adverse events.

The EGSYS (derived from patients enrolled in the Evaluation of Guidelines in SYncope Study 2 trial) Score

Predictor	Score
Palpitations preceding syncope	4
Syncope during effort	3
Heart disease/ abnormal ECG	3
Syncope while supine	2
Precipitating/ predisposing factors	-1
Autonomic prodromes	-1

This specifically identified cardiac syncope with a score of 3 or more being 99% sensitive and 65% specific for identifying cardiac syncope (positive and negative predictive values 33% and 99%). Again, I've never seen this used in clinical practice.

Investigations
A completely normal ECG makes a cardiac cause of syncope other than transient arrhythmia unlikely.

Echocardiography should be performed in any patient with a cardiac murmur and to diagnose and quantify suspected heart failure. If aortic stenosis is suspected, echocardiography should be performed urgently.
Carotid sinus massage for 5 to 10 seconds with continuous ECG and blood pressure monitoring can be used to diagnose carotid sinus syndrome. It is considered positive if it produces a drop in systolic blood pressure of 50 mm Hg or a period of asystole of 3 seconds.
Ambulatory 24 hour ECG recording may be considered in patients with a high pre-test probability of arrhythmia.
Tilt table testing is not used much any more

@drsuneet @SergioPinski @MGKatz036 To me, tilts worthless in eval of syncope. Not reproducible and high false pos/neg rates.
— Westby Fisher, MD (@doctorwes) April 6, 2014

Management
Think about all causes - 18% of patients with syncope in one study had more than one cause.

Driving - consider whether the patient should refrain from driving

Other guidelines can be found here.

Orthostatic Syncope

Orthostatic syncope (10%) is defined as an orthostatic drop of >20mm systolic blood pressure or >10 mm diastolic blood pressure. This may be due to absolute volume depletion from dehydration or haemorrhage or to venodilatation caused by medications or autonomic insufficiency (eg as occurs in Parkinson’s Disease). It is NOT the same as reflex syncope caused by orthostatic stresses, although the clinical presentation is very similar.

Pathophysiology
Sympathetic activity is chronically impaired, so vasoconstriction can't happen. This means when you stand, the BP falls.

Clinical Features
Syncope is one symptom, others include dizziness/ lightheadedness, pre-syncope; weakness, fatigue, lethargy;palpitations, sweating; (iv) visual disturbances (including blurring, enhanced brightness, tunnel vision); hearing disturbances (including impaired hearing, crackles, and tinnitus); and pain in the neck (occipital/paracervical and shoulder region), low back pain, or precordial pain.

Cardiac Causes of Syncope

There are lots of cardiac causes of syncope, and they account for 10 - 30% of syncopal episodes. Cardiac causes include: arrhythmias, cardiac failure, ventricular dysfunction (eg. hypertrophic obstructive cardiomyopathy HOCM) and valvular heart disease.

Arrhythmias
The most common cardiac causes of syncope, and the arrhythmia should be treated.
Bradycardias - Mobitz II and complete AV block are most likely to cause syncope.
Tachycardias - Narrow and Broad
Sick sinus syndrome - the sinoatrial node is damaged,because of either abnormal automaticity or sinoatrial conduction abnormalities.Syncope is due to long pauses caused by sinus arrest or sinoatrial block and a failure of escape mechanism. It is a completely different pathogenesis to carotid sinus syndrome. It is more likely to happen in people >65 years old, with ischaemic heart disease risk factors. ECGs can show many things, including sinus bradycardia.

Arrhythmia related syncope can be diagnosed on ECG in the presence of:
    Sinus bradycardia rate under 40 bpm
    Mobitz II second degree block or above
    Alternating right and left bundle branch block
    Ventricular tachycardia or rapid supraventricular tachycardia
    Pacemaker malfunction

Cardiac Failure
This will be diagnosed as normal.

Ventricular Dysfunction
The ECG needs careful scrutiny.

Valvular Problems
Aortic stenosis needs excluding. What better summary than the one from The Calgary Guide here. 

Reflex syncope

This is one of the most common causes of syncope, estimated at 35-50%, and about 30% of people have survived at least one faint - and many more will have witnessed fainting! Vasovagal syncope is the "common faint" but it can be difficult to differentiate "faints" from other causes of syncope.

Reflex syncope is neurally modulated and can be split into three main groups:
- Vasovagal (emotional eg Blood and orthostatic stress)
- Situational (cough, sneeze, defaecation, micturition, post-exercise, post-prandial)
- Carotid sinus syncope

Signs and Symptoms
Transient loss of consciousness
Jerky movements similar to a seizure
May be associated with palpitations, blurred vision, and feelings of nausea, warmth and light-headedness prior to the syncope episode, and patients are more likely to have had previous syncopal episodes.

Pathophysiology
This arises from an initial increase in sympathetic outflow followed by a rebound reduction in sympathetic activity leaving unopposed parasympathetic activity causing vasodilatation, bradycardia and hypotension.
In other word, you get worried about something, so get the flight or fight response. This then stops, and the unopposed activity makes you collapse. 

Investigations
Look for carotid sinus hypersensitivity in any patient older than 40. A ventricular pause lasting >3 seconds or fall in BP of 50mmHg defines carotid sinus hypersensitivity.


Treatment
Exercises to improve blood flow
Driving - no restriction