Headaches Flashcards
What most commonly causes subdural haematomas?
Bleed from subdural bridging veins
- forms a crescent shape on scans
When is a increase in ICP considered severe?
40mmHg
What most commonly causes subdural haematomas?
Bleed from subdural bridging veins
- forms a crescent shape on scans
What would a lesion in the posterior parietal lobe cause?
Optic ataxia: inability to move hand to a specific object using vision
Balint’s syndrome
What would a lesion in the inferior temporal cortex result in?
Visual agnosia: when a person can see but cant interpret the information
e.g. the man who mistook his wife for a hat
What should ICP be?
10mmHg
What is the tentorium?
Fold of dura mater that forms a partition between the cerebrum and cerebellum
What would cause a diffuse brain injury?
Hypoxia, meningitis
What occurs in response to an increase in ICP?
CPP decreases
BP increases and vessels dilate
ICP increases
CPP further decreases
*ultimately resulting in ischemia and infarction
*increased BP also causes bleeds to bleed more
What is uncal herniation?
Innermost part of temporal lobe can be moved towards the tentorium and put pressure on the brainstem
Which cranial nerve is affected by uncal herniation?
CN3 – causes pupillary dilation, pupil doesn’t react to light
Discuss types of brain herniation
Supratentorial:
1. uncal: temporal lobe
- central: diencephalon slips under tentorium
- cingulate/ subfalcine: cingulate gyrus squeezed to other side of brain
- transcalvarial: AKA external herniation
Infratentorial:
1. upward herniation: cerebellum displaced
- tonsillar: cerebellar tonsils slip down towards foramen magnum
Discuss uncal herniation
- Causes down and out eyes and pupil dilation
- Can compress the posterior cerebral artery and cause an ishaemic stroke in occipital lobe
- Can break basilar arteries and lead to Duret’s haemorrhages – small linear areas of bleeding in brainstem
- Causes ipsilateral weakness due to indentation on the cerebral peduncle caused by herniation on the opposite side = Kernohan’s notch
What is gaze palsy?
Eyes shift to side of lesion
Discuss staging of brain tumours
Grade 1: lesion with low proliferative potential, curative with surgical resection
Grade 2: Atypical cells, recur more frequently than grade 1, can progress to higher grades
Grade 3: evidence of malignancy, anaplastic cells, treated with aggressive chemo/radio
Grade 4: necrotic, mitotically active, neovascular, aggressive treatment, STUPP protocol (temozolomide chemotherapy + radiotherapy)
What is the STUPP protocol?
Temozolomide (alkyating agent) + radiotherapy
Used for glioblastoma
Discuss primary and secondary headaches
Primary = in the absence of significant pathology
Secondary = symptom of underlying disease e.g. infection, tumours, raised ICP
What should be examined when discussing headaches?
- Vital signs
- Fundoscopy
- Cranial and PNS examination
- Extracranial structures: neck and temporal arteries
Red flags of headaches
- New, severe, unexpected
- Reaching maximum intensiity within 5 mins- think vasculopathy e.g. bleed/ dissection
- Progressive/ persistent: possible mass lesion
- Associated features e.g. fever, seizure, neck pain, photophobia
- Aura + weakness lasting 1hr+
- Current pregnancy: pre-eclampsia?
Headaches that gets worse on standing
CSF leak - low pressure headache
Causes: spontaneous, trauma, iatrogenic
Headache worse on lying down?
Consider space occupying lesion
Headache + papilloedema
Space occupying lesion, space occupying lesion
Migraine mimics
Something that looks like a migraine but isn’t
- Trigeminal autonomic cephaliga e.g. cluster headaches: these cause people to want to move around rather than stay still
- Acute glaucoma: painful, tender, firm eye + visual loss
- Carotid artery dissection: neck pain + Horner’s
- Structural lesion: early morning headache, vomiting without nausea
- Meningitis: systemic signs and symptoms
- Giant cell arteritis: Age 50+, scalp tenderness, jaw claudication, systemic symptoms
Migraine chameleons
Something that looks like a migraine but isn’t
- TIA
- Stroke: motor loss, dysphasia
- Epilespy
- Vestibular disorders e.g. vertigo
- MS: intermittent sensory disturbance
Key difference between migrain and cluster headache?
Cluster - patient wants to keep moving, restless
Migraine - wants to stay still in dark room
Epidemiology of migraine
15-20% women
5% men
Aetiology of migraines
- Strong familial link
- Triggers: chocolate, cheese, wine
* Query is whether the foods cause migraine or whether they are part of the craving as part of the prodrome *
What causes the aura in migraine?
Wave of cortical spreading depression, decreased neuronal function
Clinical features of migraine
- Throbbing or pulsatile headache
- Develops over minutes to hours
- Light sensitivity, nausea and vomiting
- Pain aggravated by movement
- Prodrome: visual disturbance, sleepiness, food cravings, altered mood
What % of migraines occur without aura?
80%
Positive and negative symptoms of aura
Positive: zigzag lines, pins and needles
Negative: blind spots, numbness
Diagnosing migraine
3+ of the following:
- Pulsatile headache
- 4-74hr duration
- Unilateral
- N&V
- Disabling intensity
- FHx
Define chronic migraine
>15 days/month for 3 months
When to refer a patient with migraines
Any red flags
Status migrainosus
Treatment in primary care not working **important to consider medication overuse headaches first **
Investigations for migraine
Clinical diagnosis
MRI + lumbar puncture needed if:
- >50yrs and new headache
- Fever
- Thunderclap headache
- Neurological deficit
- New congitive dysfunction
- Drowsiness
- Change from normal headache
- Compromised immune system
Initial management of migraines
Lifestyle: Avoid triggers, stress management, sleep hygeine, hydration
Address comorbidities: sleep apnoea, depression, anxiety
Medication overuse: restrict medication to 2 days/ week
COCP: stop if migraines with aura
Acute treatment of migraine
1st: Simple analgesia: NSAIDs, paraceptamol, aspirin
2nd: Triptan ± NSAID e.g. sumitriptan - consider intranasal or subcut if patient vomits with migraines
Do not offer opioids or ergots
Review after 2-8 weeks
Preventative therapy for migraines
Consider if: impact on QoL and daily function e.g. 1+ per week, prologed despite treatment, acute treatment doesn’t work
Medication choice: daily propranolol, amitriptyline
*Consider treatment failed if highest dose of prophylaxis does not control migraines after 3 months - then refer to neurology
Preventing period-related migraine
Frovitriptan on days migraine is expected
Zolmitriptan
What is status migrainosus?
Attack lasting >3 days
Discuss tension-type headaches
Typical presentation: bilateral pressing or tightening, non-pulsating pain
- Mins-days
- No nausea
- Photophobia and phonphobia can occur
- Pericranial tenderness
‘A band of pain or pressure around the forehead with no neurological features’
Epidemiology of tension-type headaches
- Affects up to 80% population
- Rarely severe: most manage at home
- Affects women and young more than men and older
Aetiology of tension-type headaches
- Cause poorly understood
- stress, inappropriate eye prescription, contracted cranial muscles
What are the clinical features of tension type headaches?
Pain around forehead but no N&V or autonomic symptoms
3 types:
- Infrequent episodic: <1 day per month
- Frequent episodic: 1-14 days per month for 3+ months (+ either photophobia OR phonophobia or neither but not both)
- Chronic: 15+ days per month (+ either photophobia OR phonophobia or neither but not both) - patients with chronic TTH may also have N&V
Management of tension-type headaches
Red flags? Refer to secondary care
Episodic TTH: simple analgesia, identify comorbidities e.g. stress/ sleep disorders
Chronic TTH: consider preventative treatment e.g. 10 sessions of accupuncture, low dose amitriptyline
**Be aware of medication-overuse headaches**
**Do not offer opiods, if you think about offering opiods reconsider diagnosis**
Mechanism of amitriptyline
Tricyclic antidepressant - works as a SNRI
How do triptans work?
Agonists of 5-HT1B and 5HT1D receptors on blood vessels - causing vasoconstriction
Reduces release of nociceptive neuropeptides e.g. substance P
Discuss medication overuse headache
Headache resulting in overuse of medication e.g. ergotamines, triptansopioids, NSAIDs, paracetamol
- Headache should resolve after stopping medication
- non-steroidals and paracetamol must be taken on 15+ days per month to be considered overuse
- Opioids, triptans and ergotamine must be taken on 10+ days a month to be considered overuse
Management of medication overuse headaches
- Explain diagnosis and that withdrawal of over-used drug is mainstay of treatment
- Consider whether drug can be stopped abruptly
- Symptoms may get worse before getting better
- Review after 4-8 weeks from withdrawing medication
Discuss cluster headaches
- One of the trigeminal autonomic cephalgias
- Referred to as suicidal headaches
- Severe, unilateral periorbital pain associated with ipsilateral cranial autonomic symptoms e.g. conjunctival injection (red eye), lacrimation and eyelid oedema
Epidemiology of cluster headaches
15 per 100,000
Male predominance
Increased prevalence in close family member
Aetiology of cluster headache
- Facial pain due to activation of opthalmic branch of trigeminal nerve
- Autonomic symptoms due to activation of parasympathetic aspect of facial nerve
*Overall cause unknown*
Clinical features of cluster headache
- Hallmark is timing: occur in clusters of daily headaches for weeks or months with periods of remission
- Severe, unilateral, periorbital pain + eye symptoms
- Pain: sharp, burning, pulsating, pressure
- Attacks last 15-180 mins
- Patient cannot lie still, agitated, pacing
- Timing can often be predicted and triggers may be found e.g. alcohol, physical exertion
International classification of headache disorders - cluster headache diagnostic criteria
5+ attacks of severe-very severe unilateral orbital/ temporal pain lasting 15-180mins
+ at least one of:
- Conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, eyelid oedema, forehead/ facial swelling/ flushing, meiosis/ ptosis, restlessness/ agitation
Episodic: 80-90% cases, pain free for at least 1 month between attacks
Chronic: 10-20% cases, 12months with remission periods <1 month
Management of cluster headaches
- Exclude red flags
Lifestyle: advise re triggers, adress sleep disorders, depression etc
Acute: Sumitriptan/ zolmitriptan, 100% oxygen 12-15L through non-rebreathe mask (home oxygen can be provided)
Refer: first clsuter headache (diagnosis is made by specialist), patients often have MRI scans done, if patients develop symptoms that may suggest secondary cause, if patient is pregnant
Prevention: verapamil
What is giant cell arteritis?
AKA temporal arteritis because it most commony affects temporal artery
- Systemic vasculitis that can cause blindness - inflammation in the walls of medium and large arteries
- Uncommon
- Causes a serious headache
Epidemiology of giant cell arteritis
5-18 per 100,000 over 55yrs
- very uncommon in patients <55
4x women than men
Aetiology of giant cell arteritis
Granulomatous inflammation in walls of medium-large vessels especially superficial temporal artery
- Vasculitic lesions consist of cellular infiltrate that forms giant cells
- B cells direct antibodies to combat the vascular proteins causing inflammation in the vessels leading to narrowing and pain
Clinical features of giant cell arteritis
- 75% have a headache
- 60% have polymyalgia rheumatica (pain, stiffness and inflammation of muscles around neck and shoulders)
- Fever
- Scalp tenderness, overlying skin can be red
- Loss of pulsation over temporal artery
- Jaw claudication
- Visual loss/ double vision
How is giant cell arteritis diagnosed?
- FBC: low Hb, raised platelets
- ESR and CRP are raised in most cases (a normal level does not exclude GCA)
- Temporal artery biopsy needed for definitive diagnosis - shows intimal proliferation and narrowing of lumen + giant cells
Questions to ask if suspecting giant cell arteritis
SOCRATES
- Headache red flags
- Change in vision
- Scalp pain/ tenderness e.g. when head on pillow or combing hair
- Jaw/ tongue pain
- Polymyalgia rheumatica questions e.g. trouble turning in bed or when lifting arms
- Systemic: fever, night sweats, weight loss, anorexia
- Arm pains: limb claudication
- Chest pain
What will a FBC show in giant cell arteritis?
Low Hb (normocytic anaemia) + raised platelets
How is giant cell arteritis initially managed?
Medical emergency - treat to prevent vision loss
- Initial management is glucocorticoids - high dose prednisolone
- If patient has visual changes refer for urgen assessment by opthalmologists - they may advise giving pred in mean time
- If no visual loss, refer via urgent GCA pathway for urgent assessment with rheumatology
- Arrange for bloods
Discuss ergotamine medication for headaches
Used for cluster headaches only
Causes vasoconstriction of intracranial blood vessels by acting on 5-HT1D receptors
Used to be frequently used for migraine however this is no longer the case – known to cause medication overuse headache
Discuss management of giant cell arteritis once diagnosed
- Managed in secondary care
- Treatment 1-2yrs with glucocorticoids
- To avoid glucocorticoid toxicity methotrexate or tocilizumab may be given
- Patient reviewed every 2-8 weeks for 6 months, then every 12 weeks for 6 months then every 12-24 weeks for 12 months
- Glucocorticoid dose tapered when patient in remission but relapse is common
How is a giant cell arteritis relapse managed?
This is defined as a return of symptoms regardless of whether inflammatory markers are raised
- Visual disturbance: refer for urgent assessment
- Be aware of the fact that GCA can affect aorta and proximal branches so look out for limb claudication, abdo pain, back pain
Discuss headaches associated with raised ICP
Known as high pressure headaches (normal ICP is 7-15mmHg)
Pain occurs as excess CSF leads to stretching of meninges and activates pain-sensitive structures e.g. dura
Symptoms: headache, vomiting, transient visual changes, increased on coughing or straining, worse lying down
Causes of a raised ICP
- Mass effect: tumour
- Brain ischaemia
- Obstruction to CSF flow
- Bleed
- Infection
- Idiopathic
Clinical features of a raised ICP
Dull, generalised headache
Worsened by anything that increases ICP e.g. coughing, lying down, sneezing, bening forwards
Vomiting, papilloedema, visual changes
What is the Monroe-Kellie hypothesis?
Pressure-volume relationship between ICP, volume of CSF, blood, brain tissue and cerebral perfusion pressure
Cranial compartment is inelastic and the volume is fixed
- The fluids create an equilibrium: increase in one of the fluids leads to a decrease in another
Cerebral perfusion pressure = pressure of blood flowing to brain
CPP = MAP - ICP (therefore raised ICP leads to less blood reaching brain)
Management of raised ICP
- Treat the cause
- Lumbar puncture, ventricular drain, shunt
- If idiopathic: weight loss and acetazolamide
What causes subarachnoid haemorrhages?
Berry aneurysms (think spider body)
Presentation of subarachnoid haemorrhage
- Most commonly due to head trauma or berry aneurysm
- Peak incidence 50yrs
- Thunderclap headache (worst they’ve ever had)
- Photophobia, vomiting, loss of consciousness, deafness
- Neck stiffness
- Seizures
- Patients report prodromal symptoms: a ‘warning leak’ transient diplopia, dueen severe headache
Risk factors for subarachnoid haemorrhage
- HTN
- Smoking
- Family hx
- Autosomal dominant PKD
- Connective tissue disorders
Where do the majority of berry aneurysms occur?
95-90% in anterior circulation: mainly anterior communicating-ACA junction
Investigations for subarachnoid haemorrhage
Emergency non-contrast CT: order thin slices to avoid missing small collections of blood - sensitivity almost 100% within 6hrs of bleed - shows hyperdensity in subarachnoid space
- Patients can be agitated and need anesthetising to be scanned
U&E: hyponatremia occurs in 50% and is associated with vasospasm following SAH
- Clotting profile
- Blood glucose: hyperglycamia occurs in 1/3
- CT angio if CT negative but suspicion high
What is xanthochromia?
Yellowish discolouration of CSF occuring due to breakdown of RBCs following subarachnod haemorrhage
*This won’t be apparent straight away as it takes time for RBCs to breakdown)
How is a subarachnoid haemorrhage initially managed?
- ABC
- Isotonic saline for fluid resus
- As soon as diagnosis confirmed refer to neurosurgeons and give nimodipine (combats vasospams following SAH)
- Observe closely
- Consider seziure prophylaxis
- Give stool softener and anti-emetic after surgery as any valsalva manouvre can cause increased ICP and re-bleed
Surgical management of subarachnoid haemorrhage
- Surgical clipping: treatment of choice, mor invasive than coiling
- Endovascular coiling: platnum coils placed into aneurysm, causes thrombotic occlusion (less invasive but higher risk of re-bleed)
What is a subdural haematoma?
Collection of blood following a bleed into the space between the dura and arachnoid mater
Whick vessels are responsible for a subdural haematoma?
Bridging cortical veins that empty into the dural venous sinuses
Bridging veins = veins that transverse the dura mater and empty into the dural venous sinuses (venous drainage of the brain)
Aetiology of subdural haematomas
Chronic and acute SDH are mainly caused by trauma
- Seen in eldelry patients who have had a fall - age related brain atrophy causes veins to be more stretched and prone to bleeding
Pathophysiology of acute subdural haematomas
Usually due to shear forces disrupting bridging cortical veins
- Bleeding causes intracranial pressure to rise, cerebral perfusion pressure and cerebral blood flow decreases
- Ischaemic injury occurs
Aetiology/ pathophysiology of chronic subdural haematoma
Seen in alcohol abusers (causes brain atrophy) or those who are taking anti-coagulants or have a coagulopathy
Blood collects over >21 days and becomes symptomatic when underlying brain tissue is compressed
Presentation of a chronic subdural haematoma
Patients often have no trauma or present weeks after a fall/ trauma with vague symptoms of weakness/ confusion/ drowsiness
Classification of subdural haematoma based on timing
Acute: <3 days old (diffusely hyperdense)
Subacute: 3-21 days old (heterogenously hyperdense/isodense)
Chronic: >21 days (diffusely hypodense)
Acute on chronic: areas of hypodensity + hyperdensity
Risk factors for subdural haematoma
- Recent trauma
- Coagulopathy
- Anticoagulant medication
- 65+
- Chronic alcohol use
Key diagnostic features of subdural haematoma
Risk factors, signs of trauma on face, lacerations/ bruising on head and neck, headache (due to raised ICP), unequal pupils size (anisocoria) (due to herniation), confusion, diminished verbal response
Initial investigations for subdural haematoma
Bloods: coagulation profile, FBC
Non-contrast CT
Subdural fluid collection forms a crescent shape and may cause effacement of underlying sulci
Management of subdural haematoma
Acute: reverse anti-coagulation, craniotomy and drainage of haematoma
Chronic: can be left to spontaneoulsy recover if causing no problems, surgical manegement to remove blood either burr holes and then wash the blood out or craniotomy to remove the haematoma
What causes low-pressure headaches?
Uncommon, caused by general tears with CSF leakage, trauma, lumbar puncture or spinal anaesthetic
Characteristics of low-pressure headaches
Dull, throbbing headache made worse by standing and improved by lying down
Managamenet of low-pressure headaches
Conservative: bed rest, increased fluid intake, caffeine (causes vasoconstriction)
Epidural blood patch: blood from patient used to ‘plug’ hole in dura
What is meningitis?
Inflammation of the meninges
***Not inflammation of the brain tissue - this is encephalitis***
Which meningeal layers are most commonly affected by meningitis?
Arachnoid and pia mater (aka the leptomeninges)
How much CSF do we produce a day?
500mL, 350mL is reabsorbed into blood so we have 150mL of CSF circulating at any one time
Where is CSF found?
Between pia and arachnoid mater (subarachnoid space)
Normal to find a small amount of WBCs, proteins and glucose in the CSF
Mainly lymphocytes in the CSF with very few polymorphonuclear WBCs (e.g. neutrophils)
What can cause inflammation of the meninges?
- Autoimmune disease e.g. lupus
- Reaction to medication
- Infection (the most common across all age groups)
Routes of infection in meningitis
- Direct spread: trauma or URTI allowing infection into CSF via the skull or spinal column
- Haematogenous spread: pathogen enters blood and tracks to CSF
Age-related causes of bacterial meningitis
Epidemics (18-50yrs): n.meningitidis (meningococcus meningitis)
Head trauma: strep.pneumoniae
Immunocompromised: L.monocytogenes
<3 months: group B strep
3 months-18yrs: n.meningitidis
>50yrs: strep.pneumoniae
Which is the most aggressive and serious form of meningitis?
Bacterial
- Requires early and aggressive treatment
Epidemiology of bacterial meningitis
4/100,000 in UK per year
Peaks: infants and adolescents
Vaccinations against bacterial meningitis
Pneumococcal: protection against serious infections caused by pneumococcal bacteria, including meningitis
Hib/ Men C: protection against a type of bacteria called meningococcal group C bacteria, which can cause meningitis
Meningitis ACWY: given to freshers, protection against 4 types of bacteria that can cause meningitis: meningococcal groups A, C, W and Y.
Pathogenesis of bacterial meningitis
H.influenzae, strep.pneumoniae, n.meningitidis all colonise nasal and skull cavities
- Immunodeficiency or breach of structural defence allows bacteria into intracranial compartments
- Overtime inflammatory response occurs and polymorphonuclear cells enter CSF
- The inflammation leads to the symptoms of meningitis
CSF in meningitis
>5 WBCs in 1uL of CSF usually indicates meningitis
- The amount of WBCs in CSF indicates which type of infection is causing the meningitis:
Bacterial meningitis CSF:
- 1000s WBCs (mainly polymorphonuclear e.g. neutrophils)
- Very high opening pressure, very high protein, high lactate, <50% CSF:serum glucose ratio (bacteria use the glucose so it decreases in the CSF)
Viral meningitis CSF:
- 100s WBCs (mainly mononuclear)
- Mildly increased opening pressure, mildy raised protein, >50% CSF:serum glucose, normal lactate
What would you expect following CSF analysis of a patient with bacterial meningitis?
Very high opening pressure (>25cm H2O)
1000s of polymorphonuclear WBCs
High lactate
Very high protein levels
What is CSF opening pressure?
Pressure of CSF detected just after needle placed in spainal canal
Indicates intracranial pressure
Why does opening pressure of CSF increase in meningitis?
Presence of large numbers of WBCs - causes pressure increase
Clinical features of bacterial meningitis
- Fever
- Meningism triad (neck stiffness, photophobia, headache)
- Purpuric, non-blanching rash: suggests meningococcal septicaemia (the rash occurs because a systemic inflammatory response occurs and causes disseminated intravascular coagulopathy which causes vasodilation, capillary leakage and haemorrhaging into skin)
- Neurological complications:
- increased ICP headache, N&V
- Seizures (20%)
- Focal neuro deficits (10%)
What is meningococcal disease?
Infections caused by the bacteria n.meningitidis
Most commonly causes:
- Meningococcal meningitis
- Meningococcal septicaemia
Diagnosis of bacterial meningitis
Clinical hx, presentation and examination form initial diagnostic approach
- If bacterial meningitis is suspected, immediately commence antibiotics
- Definitive diagnosis made when microbial organism is found in CSF
When is a lumbar puncture contraindicated in meningitis?
Signs of raised ICP: GCS score <13, focal neurological signs, abnormal posturing, following seizure if not stable, dolls eye movements - this is because it could cause a drop in ICP and herniation
If rash suspicious of meningococcal septicaemia - you don’t want to introduce the infection into the CNS
Bradycardia w/ HTN, immunocompromised, systemic shock, coagulopathy, respiratory failure
Investigations for bacterial meningitis
Bloods: CRP, PCR of blood to identify causative organism
Lumbar puncture (unless contraindicated)
CSF: electrophoresis showing presence of oligoclonal bands (bands of immunoglobulins seen when analysing CSF) - presence of these in the CSF indicates CNS inflammation
Kernig’s sign: patient lies on back, flexes hip to 90o - leg straightened at knee causes back pain - pain occurs as lowering of leg stretches meninges and if they are inflamed it exacerbates pain
Management of bacterial meningitis out of hospital
Bottom line: don’t wait to give antibiotics if you suspect bacterial meningitis
If suspecting bacterial meningitis + non-blanching rah: give IV/ IM benzylpenicillin asap in part of limb that is still warm
If suspecting bacterial meningitis without non-blanching rash don’t give antibiotics unless patient will not reach hopsital urgently
Antibioitc management of bacterial meningitis in hopsital
If suspecting bacterial meningitis, give broad spectrum antibiotics immediately - don’t wait for results of investigations
- Usually a 3rd generation cephalosporin ceftriaxone
- Once species identified antibiotics adjusted
- IV antibiotics for minimum of 2 weeks
Additional treatment of bacterial meningitis
Acyclovir if suspecting encephalitis
Steroids if CSF evidently infected e.g. purulent/ high WBCs
Treat precipitating factor e.g. trauma
Supportive treatment for shock and raised ICP
Complication management e.g. drain abscess
Management of close contacts of patient with bacterial meningitis
Consult regional health protection unit
- Identify contacts who are at raisk and prescribe/ supply prophylactic treatment
**Bacterial meningitis and meningococcal disease are notifiable diseases
Which is more common, bacterial or viral menigitis?
Viral
Usually self-limiting and patients recover without major neurological complications
Epidemiology of viral meningitis
3000 cases reported each year but true incidence thought to be much higher
Most common causes of viral meningitis
Coxsackievirus B, herpes simples type II
**In most cases no organism is found**
Pathogenesis of viral meningit
Virus enters through skin lesion, GI, respiratory or urinogenital tract and then replicated locally
It then enters CNS via blood stream or by tracking along cranial/ peripheral nerve
Clinical features of viral meningitis
Similar presentation to bacterial meningitis but less severe
- Seizures, focal neurological deficits
Profound changes in consciousness are rare in viral meningitis (if present, suspect encephalitis)
Investigations for viral meningitis
- Difficult to culture viruses from CSF
- Often a clinical diagnosis as difficult to identify organism
- Viral meningitis can be distinguished from bacterial via CSF analysis (viral = lower WBCs in 100s, normal lactate, mild protein increase)
Management of viral meningitis
- Benign, self limiting condition
- If a headache perists + visual impairment there may be impaired CSF reabsorption following inflammation - this can lead to raised ICP
- CSF diversion procedures can be carried out to relieve the ICP
What is encephalitis?
Inflammation of the neuronal and glial substance of the brain (the brain parenchyma)
- Can be caused by infectious agents or by an autoimmune process
Most common cause of viral encephalitis
HSV1 - early treatment with aciclovir reduces from 70% to 20-30%
Epidemiology of encephalitis
1 in 100,000 annually
Aetiology of encephalitis
Most commonly identified cause is HSV1 - >90% cases
Immunocompromised patients: CMV, HIV, JC viruses
Pathogenesis of encephalitis
- Organism enters body via inhalation/ other
- Gains access to CNA via olfactory mucosa and cranial nerves leading to diffuse inflammation in basal frontal and medial temporal lobes
Clinical features of encephalitis
- Headache, fever, seizures, focal neurological deficits, significant mental status deterioration, photophobia, phonophobia, nuchal rigidity (neck stiffness)
There may be a prodrome but HSV1 encephalitis often doesn’t have a prodrome
Diagnosis of encephalitis
Evidence of inflammation following CSF analysis + clinical ± radiological evidence of focal brain involvement
CSF in viral encephalitis is similar to that of viral meningitis
90% patients have an abnormal brain MRI - findings depend on cause but often shows hyperdensity with T2/ FLAIR sequences
Management of encephalitis
Without treatment HSV encephalitis has a high morbidity and mortality so most clinicians start acyclovir in patients presenting with features suggestive of encephalitis
- IV acyclovir given for a minimum of 2 weeks
- If caused by autoimmune condition, responds to IV steroids
Prognosis of encephalitis
Worst outcome with HSV1 - untreated has a 70% mortality and most patients are left with persistent neurological deficits
What is posterior reversible encephalopathy syndrome?
Swelling of caudal part of brain
Characterised by headache, seizures, altered mental status and visual loss
Imaging shows white matter vasogenic oedema affecting the occipital and posterior parietal lobes only
Causes: HTN, kidney disease, infection, pre-eclampsia
Patient with a thunderclap headache but they have a negative CT head - what’s next?
The negative CT head does not exclude subarachnoid - they need a lumbar puncture after 12hrs to look for evidence of blood in the CSF
Patient presents weeks after what you think sounds like a subarachnoid haemorrhage - what di we do?
Gradient echo - MRI sequence
Angiogram
How common is low pressure headache after lumbar puncture?
3/10 people will experience this
Most common complication of meningitis?
Sensorineural hearing loss
