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Headache Flashcards

1
Q

How common are headaches?

A

One of the most common symptoms

Symptoms are unpleasant, disabling and common worldwide and have substantial economic impact due to time lost from work

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2
Q

What is a primary headache?

A

No underlying cause relevant to headache

Migraine, cluster, tension

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3
Q

What is a secondary headache?

A

A headache with underlying cause

Need to identify underlying cause eg giant cell arteritis

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4
Q

What are the red flags for secondary headache?

A 
HIV/immunosuppressed
Fever
Thunderclap headache
Seizure and new headache
Suspected meningitis
Suspected encephalitis
Red eye - acute glaucoma
Headache + new focal neurology eg papilloedema
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5
Q

Give an example of a secondary cause of secondary headache?

A

Meningitis
SAH
GCA
Medication overuse headache

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6
Q

Name another type of headache

A

Trigeminal neuralgia

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7
Q

What is a cluster headache?

A

Most disabling of primary headache disorders

Headache causing excruciating pain around one eye, temple or forehead

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8
Q

How common are cluster headaches?

A 
Distinct from migraines
Much rarer than migraines 1 per 1000
More common in men
Affects adults between 20-40
Commoner in smokers
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9
Q

What can increase your risk of getting cluster headaches?

A

Smoker
Male
Autosomal dominant gene has role

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10
Q

What is the pathology of cluster headache?

A

Unknown
Superficial temporal artery smooth muscle hyper-reactivity to serotonin
Hypothalamic grey matter abnormalities

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11
Q

How do cluster headaches present?

A

Sudden onset of excruciating pain around on eye, temple or forehead
Ipsilateral cranial autonomic features
- Eye may become watery and bloodshot with lid swelling and lacrimation
- Facial flushing
- Rhinorrhoea
- Miosis +/- ptosis
Pain unilateral and almost always affects same side
Rises to crescendo over minutes lasts 15-160 mins, one/twice per day - usually at same time
Nocturnal/early morning
+/- vomiting
Episodic - clusters last 4-12 weeks and followed by pain-free periods of months or even 1-2 years before next
Can be chronic (last for more than 1 year without remission)

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12
Q

What could be a differential diagnosis of cluster headaches?

A

Migraine

SAH

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13
Q

How are cluster headaches diagnosed?

A

Clinical diagnosis
Rule out differentials
At least 5 headache attacks fulfilling above criteria

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14
Q

How can you treat an acute attack of cluster headaches?

A

Analgesics don’t help
100% 15L for 15mins via non-rebreathable mask
Triptan

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15
Q

How can you prevent cluster headaches?

A

CCB eg verapamil first line
Avoid alcohol
Corticosteroids can help

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16
Q

What is a migraine?

A

Recurrent throbbing headache often preceded by aura and associated N&V, and visual changes

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17
Q

What might you get in a migraine aura?

A 
Fortification spectra (zig-zag lines)
Shimmering
Scotomas (black holes in visual field)
Results in pins and needles
Dysphasia
Weakness of limbs and motor function
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18
Q

How common is migraine?

A

Most common cause of episodic recurrent headache
More common in women
90% onset before 40
If > 50 then pathology sought
Usually severity decreases with advancing age

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19
Q

What can trigger a migraine?

A 
CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult - loud noise
Exercise
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20
Q

What might cause a migraine?

A

Brain chemical imbalance

Changes in brainstem and interactions with trigeminal nerve

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21
Q

What can increase your risk of migraine?

A

Strong genetic component - FHx
Female
Age - can occur at any age but majority have first migraine in adolescence

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22
Q

What is the pathology of migraine?

A

Genetic and environmental factors play role
Genetics - neuronal hyper-excitability
Changes in brainstem blood flow lead to unstable trigeminal nerve nucleus and nuclei in basal thalamus
Cortical spreading depression - self-propagating wave of neuronal and glial depolarisation spreading across cerebral cortex thought to cause aura of migraine and leads to release of inflammatory mediators impacting on trigeminal nerve nucleus
Results in release of vasoactive neuropeptides including calcitonin gene related peptide and substance P - results in process of neurogenic inflammation - vasodilation and plasma protein extravasation leading to pain the propagates all over cerebral cortex

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23
Q

What might you get before a migraine and what might it entail?

A

Prodrome hours/days before - yawning, cravings, mood/sleep changes
Aura
- Visual - chaotic cascading, jumbling, distorting lines, dots, zigzags, scotoma, hemianopia
Somatosensory
- Paraesthesia spreading from fingers to toes

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24
Q

How does a migraine present?

A 
Attacks lasting 4-72 hours
Two of the following
- Unilateral 
- Pulsing
- Moderate/severe pain
- Aggravated by routine physical activity
During headache at least one of
- Nausea and/or vomiting 
- Photophobia and phonophobia
Not attributable to another disorder
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25
How might a migraine with aura present?
At least 2 attacks Aura precedes attack by minutes and may persist during it Unilateral, pulsatile headache
26
What could be a differential diagnosis of migraine?
``` Tension headache Cluster headache Medication over-use headache Meningitis/SAH if sudden Thromboembolic TIA Brain tumour Temporal arteritis ```
27
How do you diagnose migraine?
Clinical diagnosis
28
What might you examine to rule out other differentials?
Eyes - papilloedema and other eye issues BP Head and neck (scalp, neck muscle and temporal arteries)
29
What tests might you do to rule out other differentials?
CRP and ESR MRI/CT if red flags LP
30
When would you do an LP?
Worst headache of life Severe rapid onset headache Progressive headache Unresponsive headache
31
How do you treat migraine?
``` Reduce triggers Acute - Triptans - NSAIDs - +/- anti-emetic Prevention - Beta-blocker/tricyclic antidepressant/anti-convulsant if > 2 attacks per month or acute treatment required > 2x per week ```
32
What are the side effects of triptans?
Arrhythmias Angina MI
33
When are triptans CI?
IHD Coronary spasm Uncontrolled high BP
34
What is a tension headache?
Most chronic daily and recurrent headaches are tension headaches
35
How common are tension headaches?
Commonest primary headache Can be episodic < 15 days/month or chronic > 15 days/month for at least 3 months No organic cause
36
What can cause tension headaches?
``` Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise ```
37
How do tension headaches present?
``` Usually has one of the following - bilateral, pressing/tight non-pulsatile, mild/moderate pain, +/- scalp muscle tenderness No vomiting/sensitivity to head movement No aura Not aggravated by physical activity Tight band-like sensation Pressure behind eyes Last from 30 mins to 7 days Not attributed to another disorder ```
38
What could be a differential diagnosis for tension headaches?
Migraine Cluster GCA Drug-induced
39
How are tension headaches diagnosed?
Clinical
40
How can you treat tension headaches?
``` Reassurance and lifestyle advice Stress relief Symptomatic treatment - Aspirin/paracetamol/NSAIDs Limit analgesia to prevent medication overuse ```
41
When might you get medication over-use headaches?
Worsens whilst on regular analgesics espec opioids | Other causes are mixed analgesics
42
What is trigeminal neuralgia?
Chronic, debilitating condition resulting in intense and extreme episodes of pain
43
What are the branches of the trigeminal nerve?
1 - ophthalmic 2 - maxillary 3 - mandibular
44
How common is trigeminal neuralgia?
``` Peak incidence between 50-60 More common in women Prevalence increases with age May be due to genetic predisposition Almost always unilateral ```
45
What is the cause of trigeminal neuralgia?
Compression of trigeminal nerve by a loop of vein or artery Local pathology - aneurysms, meningeal inflammation, tumours eg vestibular schwannoma - local pathology more common in younger people as cause of compression 5th nerve lesion due to pathology - With brainstem - tumour, multiple sclerosis, infarction - At cerebellopontine angle - acoustic neuroma, another tumour - Within petrous bone - spreading middle ear infection - Within cavernous sinus - aneurysm of internal carotid, tumour or thrombosis of cavernous sinus
46
What can increase your risk of trigeminal neuralgia?
Hypertension | Triggers - washing affected area, shaving, eating, talking, dental prothesis
47
What happens when the nerve is compressed in trigeminal neuralgia?
Demyelination and excitation of nerve resulting in erratic pain signalling
48
How does trigeminal neuralgia present?
Almost always unilateral At least 3 attacks of unilateral facial pain Facial pain occurring in one or more distribution of trigeminal nerve, with no radiation beyond trigeminal distribution Pain has at least 3 of the following - Reoccurring in paroxysmal (sudden and frequent) attacks from a fraction of a second to 2 minutes - Severe intensity - Electric shock like, shooting, stabbing, or knife-like - Precipitated by innocuous stimuli by affected side of face eg washing or shaving
49
What are the differential diagnoses of trigeminal neuralgia?
``` GCA/temporal arteritis Dental pathology Temporomandibular joint dysfunction Migraine Cluster headaches ```
50
What is the diagnosis of trigeminal neuralgia?
Needs to be at least 3 attacks with unilateral facial pain Clinical diagnosis based on above criteria and based on history MRI to exclude secondary causes or other pathologies Not attributed to another disorder
51
What is the treatment of trigeminal neuralgia?
Typical analgesics and opioids don't work Anticonvulstants eg oral carbamazepine Less effective - phenytoin, gabapentin, lamotrigine May spontaneously remit after 6-12 months If drugs fail then surgery - Microvascular decompression - anomalous vessels separated from trigeminal root - Gamma knife surgery - directly at trigeminal nerve ganglion or nerve root - Stereotactic radiosurgery
52
What can cause temporal arteritis?
Giant cell arteritis
53
What is giant cell arteritis?
Inflammatory granulomatous arteritis of large cerebral arteries as well as other large vessels
54
How common is GCA?
Primarily in those over 50 Incidence increases with age More common in women
55
What can increase your risk of GCA?
Over 50 Female RA, SLE, scleroderma
56
What is the pathology of GCA?
Arteries become inflamed, thickened and can obstruct blood flow
57
What arteries are most likely to be affected in GCA?
Cerebral arteries - Temporal artery - Ophthalmic artery
58
How does GCA present?
``` Severe headaches (temporal pulsating) Tenderness of scalp or temple Claudication of jaw when eating Tenderness and swelling of one or more temporal or occipital arteries Sudden painless vision loss - emergency Malaise Lethargy Fever Dyspnoea Morning stiffness Unequal or weak pulses ```
59
What could be a differential diagnosis of GCA?
Migraine Tension headache Trigeminal neuralgia Polyarteritis nodosa
60
How do you diagnose GCA?
``` 3 or more of - Over 50 - New headache - Temporal artery tenderness/decreased pulsation - ESR raised - Abnormal artery biopsy - inflammation infiltrates present Normochromic, normocytic anaemia Raised ESR ANCA very high CRP very high Serum alkaline phosphatase raised Temporal artery biopsy ```
61
How do you treat GCA?
High dose steroid - prednisolone to prevent vision loss - gradual reduction of steroids over 12-18 months Used long term so GI and bone protection Monitor treatment by ESR/CRP
62
What can cause raised intracranial pressure?
``` Bleeds Tumour Stroke - oedema/haematoma Aneurysm Hypertension Brain infection Idiopathic intracranial hypertension Meningitis or encephalitis Abnormal blood vessel - arteriovenous fistula or arteriovenous malformation Venous sinus thrombosis Chiari malformation Vasculitis ```
63
How does raised intracranial pressure present?
``` Headache Blurred or temporary loss of vision Feeling less alert than usual N&V Fatigue Irritability Changes in behaviour Weakness/problems with moving or talking Present on waking - worse in morning, may improve on standing up Made worse by coughing, sneezing, straining Papilloedema ```
64
How is raise ICP diagnosed?
Neuroimaging - to rule out mass lesions, venous sinus thrombosis, hydrocephalus LP - measure opening pressure
65
How do you treat raised ICP?
Treat underlying cause Diuretics Carbonic anhydrase inhibitors - acetazolamide (reduces CSF production) LP Surgery - shunts, protection of optic nerve
66
What is idiopathic intracranial hypertension?
Build up of pressure around brain that is attributed to no other cause
67
What can increase your risk of getting IIH?
``` Young, overweight, female Polycystic ovary disease Cushing's Hypoparathyroidism Hypo/hyperthyroidism Medications - some antibiotics, steroids, combined OCP Iron deficiency anaemia Polycythaemia Lupus ```
68
What causes IIH?
Reduced CSF resorption
69
How does IIH present?
``` Headaches Transient visual obscuration due to papilloedema 6th nerve palsy CSF pressure elevated Brain imaging normal ```
70
What must you do when someone presents with symptoms of raised ICP?
Look at eyes CT/MRI THEN LP
71
How is IIH diagnosed?
Rule out other differentials
72
How can you treat IIH?
Weight loss Stop medications causing symptoms Diuretics Carbonic anhydrase inhibitors eg acetazolamide Short course steroids Regular LP Surgery - shunts, protection of optic nerve
73
What is hydrocephalus?
Build up of fluid in brain causing extra pressure to be exerted on brain which can cause damage
74
What is normal pressure hydrocephalus?
Triad of symptoms - Difficulty walking - Urinary frequency urgency, incontinence - Mental slowing (mild dementia)
75
What can cause hydrocephalus?
``` Haemorrhage Thrombosis Meningitis (particularly TB) Brain tumours - posterior fossa and brainstem obstructing aqueduct or 4th ventricle outflow Head injury Stroke Idiopathic 3rd ventricle colloid cyst Choroid plexus papilloma - rare but secretes CSF ```
76
How does hydrocephalus present?
``` Headache Neck pain N&V Sleepiness - can progress to coma Changes in mental state such as confusion Blurred or double vision Difficulty walking Urinary and bowel incontinence Ataxia ```
77
How can you diagnose hydrocephalus?
``` CT/MRI Assessment of gait/mental ability LP Lumbar drainage test Lumbar infusion test ```
78
How is hydrocephalus treated?
Shunt surgery | Endoscopic third ventriculostomy
79
What is meningitis?
Inflammation of the meninges of the brain | Often implies infection
80
How common is meningitis?
Occurs in people of all age groups but more common in infants, young children, and the elderly Meningococcal disease is a notifiable disease
81
What are the main causes of meningitis in adults and children?
Neisseria meningitides - gram negative diplococci - droplet spread Strep pneumoniae or pneumococcus Less common - H influenzae due to vaccine
82
What is the main cause of meningitis in pregnant women/older adults?
Listeria monocytogenes - found in cheese
83
What are the most common causes of meningitis in neonates?
E coli | Group B haemolytic strep eg streptococcus agalacticae
84
What is the most common cause of meningitis in the immunocompromised?
``` Cytomegalovirus Cryptococcus neoformans (fungi) TB HIV HSV ```
85
What bacteria can cause meningitis?
``` Neisseria meningitides Strep pneumoniae Strep aureus Group B strep Listeria monocytogenes Gram negative bacilli eg E coli TB Teponema pallidum ```
86
What viruses can cause meningitis?
``` Enterovirus - ECHO, coxsackie Mumps HSV HIV EBV ```
87
What fungi can cause meningitis?
Cryptococcus neoformans | Candida albicans
88
What are the non-infective causes of meningitis?
Malignant meningitis Intrathecal drugs Blood following SAH
89
What can increase your risk of getting meningitis?
``` Intrathecal drug administration Immunocompromised Elderly Pregnant Bacterial endocarditis Crowding eg military base, university students Diabetes Malignancy IVDU ```
90
How can microorganisms reach the meninges?
Direct extension - from ears, nasopharynx, cranial injury, congenital meningeal defect Bloodstream
91
How do you get meningococcal septicaemia?
Bacteria invade into blood Presence of endotoxin on bacteria leads to inflammatory cascade Petechial rash + signs of sepsis
92
What does the pia arachnoid look like?
Congested with polymorphs (neutrophils) | Layer of pus forms which may organise to form adhesions leading to cranial nerve palsies and hydrocephalus
93
What does chronic meningitis with TB look like?
Brain covered in viscous grey-green exudate with numerous meningeal tubercles
94
What does viral meningitis look like?
Predominantly lymphocytic inflammatory CSF reaction without pus formation Little or no cerebral oedema unless encephalitis develops
95
What is the triad of symptoms of meningitis?
Headache Neck stiffness Fever
96
What is the clinical presentation of acute bacterial infection causing meningitis?
Onset sudden Papilloedema usually bilateral can occur over hours to weeks due to raised ICP Intense malaise, fever, rigors, severe headache, photophobia, vomiting Irritable and preferring to lie still Neck stiffness, positive Kernig's and Brundzinski's sign Septicaemia - non-blanching petechial and purpuric skin rash Altered mental state and GCS Seizures and focal CVS signs Progressive drowsiness, materialising signs and cranial nerve lesions indicated complications
97
What complications can you get in meningitis?
``` Venous sinus thrombosis Severe cerebral oedema Cerebral abscess Hearing loss Seizures Developmental problems ```
98
What is viral meningitis?
Benign self-limiting condition lasting 4-10 days | Headache may follow for some months
99
What can cause chronic meningitis and what are the symptoms?
TB Long history of vague symptoms - headache, anorexia, vomiting Signs of meningeal triad often absent/late
100
What could be a differential diagnosis for meningitis?
Aseptic meningitis (due to tumour) SAH Encephalitis
101
How do you diagnosed meningitis?
``` Blood cultures before LP Bloods - FBC, U&E, CRP, glucose LP - if unable to perform within 30 mins give empirical antibiotics - Send for microscopy and sensitivity CT head - exclude lesions Throat swabs Pneumococcal and meningococcal serum PCR Don't do LP with non-blanching rash ```
102
What would the LP for bacterial meningitis look like?
Neutrophils, raised protein, low glucose, turbid colour
103
What would the LP for viral meningitis look like?
Lymphocytes, normal protein and glucose
104
What would the LP for TB meningitis look like?
Lymphocytes, raised protein, low/normal glucose
105
What are the indications for CT before LP in suspected meningitis?
``` Age > 60 Immunocompromised Hx of CNS disease New onset/recent seizures Decreased conscious level Focal neurological signs Papilloedema ```
106
How do you treat meningitis?
If suspect bacterial start antibiotics before tests come back IV benzylpenicillin/cefotaxime if septicaemia IV cefotaxime/ceftriaxone - 3rd gen cephalosporins IV chloramphenicol if severe anaphylaxis to penicillin Over 50/immunocompromised - add IV amoxicillin to treat listeria Consider steroids to reduce cerebral oedema IV vancomycin if recently travelled
107
What prophylaxis do you give to contacts?
Oral ciprofloxacin stat | Oral rifampicin - can't give to pregnant women
108
What is encephalitis?
Infection and inflammation of brain parenchyma
109
How common is encephalitis?
Most frequent in children and elderly - mainly viral cause | More common in immunocompromised
110
What are the viral causes of encephalitis?
``` HSV 1 and 2 Varicella zoster EBV Cytomegalovirus HIV Mumps Measles Enteroviruses Adenoviruses ```
111
What are the non-viral causes of encephalitis?
Bacterial meningitis TB Malaria
112
What are the causes of autoimmune encephalitis?
Paraneoplastic limbic encephalitis Voltage-gated potassium channel limbic encephalitis Anti-NMDA receptor anti-body encephalitis
113
What can increase your risk of encephalitis?
Extremes of age | Immunocompromised
114
What is the pathology of encephalitis?
Disease mostly affecting the frontal and temporal lobes resulting in decreased consciousness, confusion, and focal signs
115
How does encephalitis present?
Whole brain affected - problems with consciousness Insidious onset over days or can be abrupt Triad - fever, headache, altered mental status Begins with features of viral infection - fever, headaches, myalgia, fatigue, nausea Progresses to personality and behavioural changes, decreased consciousness, drowsiness and confusion Focal neurological deficit - hemiparesis, dysphasia, seizures, raised ICP, midline shifting = coning, coma Hx of travel and/or animal bites
116
What are the differentials of encephalitis?
Meningitis Stroke Tumour
117
What investigations should you do in suspected encephalitis?
MRI - areas of inflammation and swelling, generally in temporal lobes in HSV encephalitis, midline shifting EEG - period sharp and slow wave complexes LP - high lymphocytes, PCR Blood and CSF serology
118
How is encephalitis treated?
If viral - acyclovir before investigation results 10mg/kg TDS for 14-21 days Early treatment can reduce mortality and long term damage Anti-seizure medication eg primidone
119
What are the complications of encephalitis?
Memory impairment Personality change Epilepsy
120
What are the symptoms of limbic encephalitis?
Facio-branchial dystonic seizures, confusion, agitation, hyponatraemia
121
What is paraneoplastic limbic encephalitis?
Seen with small cell lung cancer and testicular tumours Associated with variety of antibodies inclu anti-Hu and anti-Ma2 MRI - high hippocampal signal Precedes diagnosis of cancer in most cases and should prompt investigations
122
What is voltage-gated potassium channel limbic encephalitis?
``` Produce a variety of disorders Usually occurs in patients over 50 Can be associated with thymoma (v rare) Treatment - high dose steroids Neuromyotoninand peripheral nerve hyperexcitability syndromes seen with antibodies to VGKC ```
123
What is anti-NMDA receptor antibody encephalitis?
Limbic encephalitis followed by coma and status epilepticus Orofacial dyskinesias characteristic Patients usually younger and most have teratomas eg ovarian May respond to immunotherapy - IV Ig or plasma exchange initially, followed by steroids, rituximab or cyclophosphamide

Neuro and geriatrics (21 decks)

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