Headaches Flashcards
List primary headache disorders
1: Migraine 2: tension type headache 3: cluster headache and trigeminal autonomic cephalagias 4: other primary headaches
Can be considered as
- tension
- Traction
- inflammation
- vascular process
Discuss pathophysiology of migraine
was thought to be vascular in origin however this has been disproved. Vascular changes are thought to be a epiphenomenon of what is an underlying primarily neurological event Abnormal tirgeminal nerve activation possibly triggered by cortical spreading depression leads to pain and sensitization of higher order neurons in the brainstem and thalamus
Discuss retinal migraines
rare syndrome consisting of recurrent attacks of monocular visual dysfucntion and may include positive features such as scintillations or negative features such as blindness. As with all migraines is completely reversible
Discuss hemiplegic migraine
characterized by a motor aura include hemiplegia and hemiparesis. Neurological symptoms can last up to 60 minutes followed by a headache. Rarely the motor deficit is persistent a consequence of a true migrainous stroke
Discuss brainstem migraine
common neurolgoical finding include dysarthria, tinnitus, vertigo, diplopia and ALOC
List triggers for migraine headaches
sleep deprivation stress hunger hormonal changes including menstruation OCP nitroglycerin
Discuss abortive therapies for migraines
For mild to moderate attacks simple analgesics are often effective. Gastric stasis is often present in true migraines and may limit the effectiveness of oral agents. Prokinetics such as metoclopramide may aid in absorption and make treatment more effective. Dopamine antagonists such as prochlorperazine, metoclorpamide and droperidol are highly effective as a monotherapy for acute migraine attacks. Sumatriptan is a selective 5ht agonist and can be effective in treating headache. Common side effects of triptans include chest pain, throat tightness, flushing. Do not use in pregnancy, htn, CAD Can use dexamethasone 10mg to reduce re-presentation of migrainous patients
Sphenopalitine blocks can be useful for the treatment of acute migrainous headache. 1ml of 1% lidocaine areoroslized using an atomizer .
Discuss cluster headaches
Cluster headache is the only headache syndrome that is more common in men then in women. Headache tend to occur repeatedly during a specific period of time interval. Several precipitating factors have been identified include the ingestion of alcohol, stress and climate change. As with migraine abnormal activation of the trigeminal nerve contributes to headache nocioception. Secondary parasympathetic activation causes typical associated symptoms such as rhinorrhea and lacrimation.
Discus clinical features of cluster headache
Occur suddenly with little warning. Multiple episodes often occur in a 24 hour period. Episodes can last from 15minutes to 3 hours Pain is typically unilateral stabbing pain to the eye which may awaken patient from sleep. Symptoms occur specifically in a trigeminal distribution Patient present agitated, ancious rocking rubbing the head and pacing. Attucks often subside rapidly leaving the patient exhausted. Can have ipsilateral autonomic symptoms such as ptosis, miosis and forehead or facial sweating.
Discuss DDX of cluster headaches
Carotid artery dissection which should be excluded in patients who present with unilateral face or neck pain and Horners syndrome. Trigeminal neurolgia – pain peaks within seconds and usually only last a few minutes. rare trigeminal autonomic cephalagias
Discuss management of cluster headaches
High flow oxygen is first line– delievered through a non rebreather at a rate of 12 L/min it aborts the headache within 15 minutes in 80% of patients. Subcut sumatriptan can be tiralled. Once presenting headache has been managed need to try to reduce further headache – use of prednisone 100mg for 5 days with a 12 day taper is recommened. Verapamil can be consided 120mg TDS
Discuss tension headache
Most common recurrent headache disorder but a rare cause for ED presentation. Women are affected slightly more then men. By definition episodic tension type headache can last as little as 30 minutes and as long as 7 days. PAtients typicall present with a tight bandline discomfort around the head that is nonpulsating and dull.
Discuss subarachnoid haemorrhage
80% of patient with nontraumatic SAH have a ruptured saccular aneurysms. Other causes include AVMs, cavernous angiomas, mycotic aneuroysms, neopalsms and blood dyscrasias. Most cases of SAH occur between the ages of 40-60 80% of patient will have a thunderclap headache described as the worst headache of my life. 20% of patient will have onset with exertion, valsalva or sex Peaks within seocnds to minutes – associated features include syncope, neck-stiffness, nausea and vomiting, photophobia and seizures. Signs depend on the extent of the SAH. Meningismus is present in more than 50% of patients and up to 20 % have neurology. 3-rd or 6th nerve palsy can be present. Up to 30% of patient recall a sentinel headache several days earlier
Discuss the Hunt and Hess scale of subarachnoid haemorrhage
stratifies patients according to their clinical signs and symtpoms patients with grade 1 or grade 2 haemorrhage have good prognosis those with grade 4-5 tend to do poorly - mortality
Grade 0 - unrurpauted aneurysm wihtout symptoms 0% mortality
Grade 1- asymptomatic or minimal heache with slight nuchal rigidity - 1-3%
Grade 1 a- no acute menigneal or brain reaction but with fixed neuro deficit 1-3%
Grade 2- Moderate to severe headache nucahl rigidity no neurlgoical deficit other than CN palsy 3-55
Grade 3- drowsy confused or mild deficit 9-19%
Grade 4 Stupor moderate to severe hemiparesis, possible early decorticate rigidity and vegetative disrubtances 23-42%
Grade 5- deep coma decerebrate rigidity moribund 70-77%
List a DDX for SAH headache
carotid artery dissection, cerebral venous thrombosis, reversible cerebral vasoconstriction syndrome, haemorrhagic or ischaemic stroke and primary headache disorders.
Discuss diagnostic testing of SAH
CT scan urgently sensitivity is for SAH is greater then 90% however this reduces to les then 50% by the end of the first week.
There is one well designed study taht showed 100% sensitiviyt and specificity for CT if performed within 6 hours time.
Current guidlines are still to perform LP for xanthochromia if suspected.
To differentiate a traumatic LP from a SAH the patients CSF is spun and the supernatant observed for xanthochromia. This yellowish pigmentation is secondary to the metabolism of HB a proces that can take up to 12 hours to occur.
If diagnosis is confirmed a CTA should be ordered – this is a reasonable first line in low risk patient, those who refuse LP who are still reasonable high risk for SAH,.
Up to 90% of patients with SAH have a cardiac arrhythmia or ECG abnormalities suggestive of acute cardiac ishcaemia. Typical finding include ST-T wave chagnes, u waves and QT prolongation
Discuss management of SAH
Primary goals a aimed at treating acute medical and neurological complications, preventing recurrent ahemorrhage and forestalling ischaemic complications of vasospasm.
As grade 3 SAH and higher are at risk of resp failure and hypercapnia which can worsen ICP early intubation is often necessary for these patients.
PREVENTION OF DELAYED CEREBRAL ISCHAEMIA: Nimodipine should be started as soon as possible post diagnosis to prevent spasm. Oral dosage is 60mg by mouth or NG every 4 hours. Should have HD monitoring at this stage. Antifibrinolytics (aminocaproic acid) is used to reduce the risk fo early rebleeding
Bp management is determined by patient clinical status, in general a BP less then 160 and a MAP less then 130mmhg unless vasospastic.
Use labetalol or hydralzine. Vasodilators such as snip or GTN should be avoided due to a propensity to cause increase cerebral blood volume and increase ICP.
Discuss Giant Cell Arteritis
inflammatory vasculopathy that occurs in medium and large arteries. Typically involves the large branches of the aorta and has a predilection for the extracranial branches of the carotid (temporal and occipital)
Mean age of onset is 71 year old and is rare before 50
Women are more commonly affected then men. In the majority of cases loss of vision is due to arteritic anterior ischemic optic neuropathy.
Headache is the most common initial features and occurs in more then 70% of patients. Headache is often 2-3 months in duration and can be intermittent. Usually is localised to the temporal region. Jaw claudication secondary to vascular insufficiency of the masseter and temporalis muscles.
Sysetmic features are often present including fever, anorexia and weight loss. 40% of patient develop syhmtpoms of polymyalgia rheumatica
The most serious complication of GCA is permenant vision loss amaruosis fugax can occur before permanent vision loss.
Signs including tenderness or reduced or absent pulses to the temporal artery with erythema and nodularity or swelling. VA, fields and fundoscopy should be performed. The presence of relative afferent pupillary defect should icnrease the suspcifion of GCA.
Discuss diagnosis and mangement of GCA
Majority of patient will have a significantly raised ESR usually to more than 50mm/hr and often more than 100mm/hr as well as raised CRP, thrombocytosis and anaemia. Relatively poor specficity and sensititvity however only 4% of patient with GCA will have a normal ESR and CRP.
Can consider doppler US of the temporal arteries revealing a peri-luminal hypoechoic halo
The only test that confirms a diagnosis of GCS is a temporal artery bopsy
Those with amaurosis fugax or diplopia with TA need to start urgent glucocorticoids as they are at risk of permanent visual loss. Those with visual symptoms should have a methyl pred burst 100mg per day for 3 days.
Discuss carotid and vertebral artery dissection
CAD causes approximatly 2% of strokes and in patient under 50 years of age is the most comon cause of ischaemic stroke.
May occur suddenly but is usually seen with an assocaited sudden neck movement or trauma. Reported mechanims invldue neck torsion, chiro, coughing heavy lifting interecourse or child birth.
The typical presentaiton of CAD is that of abrupt onset of pain in the head or neck often in association with symtpoms resulting from aischaemic consequences of the diessection and emboli. Neurology secodnary to cerebral ischaemia usually occur within the first few hours follwoign the onset of the headache or neck.
Discuss carotid artery dissection
Classic triad is unilateral headache or neck pain sometimes radiating to the unilateral eye, ipsilateral parital horner’s syndrome and either blindness due to retinal ischaemi or contralateral motor deficits.
Acute severe retro-orbital pain in a previosuly healthy person with nil history of cluster is suggestive of carotid dissection.
Discuss Discuss vertebral artery dissection
Less common then carotid dissection. Classic presnetation is that of a relatively young person with sever unilateral posterior headache and a rapidly progressive neurological deficit with sympomts of brainstem and cerebella ishcaemia.
Common finding including veritgo, severe vomiting, ataxia, diplopia, hemiparesis unilateral facial weakness and tinnitus.
Discuss cerebral venous thrombosis
Thrombosis of the intracranial veins and sinuses is a rare disorder causing approximatly 1% of all strokes. Typically present with headache disproportionately affecting younger individuals
Mulitple causes and risk factors are classically linked to the Virchows triad. Both genetic and acquired prothrombotic conditions have been assoicated with CVT. Acquired causes include pregnancy and the puerperium, malignancy, head trauma, surgery, paramengieal infection and th OCP.
Discuss clinical features of central venous thrombosis
Two major categories
1: those caused by increased ICP due to reduced venous drainage
2: those related to focal brain injury resulting in ischaemia infarction or haemorrhage
Diffuse headache increasing in severity over days to weeks is the most common symptom. Focal neurolgocial findings when present are related to the region of brain affected. Siezure both generalised and focal frequently occur. Occular finding including orbital pain, proptosis, chemosis extraocular msucle paralysis and papilloemea.
D-dimer can be used in those with low risk to exclude CVT
MRV is gold standard, CTV/A can be used in patient in whom an MRI is contraindicated or not available.
