Neuro 3 Flashcards
What is the difference between primary and secondary headaches?
Primary - no abnormality behind, just occur
>Tension type, cluster + migraines
Secondary - some sort of pathology behind it
>Not all are sinister
What are tension type headaches?
Most frequent type, but not disabling
Mild, bilateral headache - often pressing or tightening in quality
What is the abortive treatment for tension type headaches?
Aspirin or paracetamol
NSAIDs
Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache
What is the preventative treatment of tension type headaches?
Rarely required
Tricyclic antidepressants
>amitriptyline, dothiepin, nortriptyline
What is a migraine?
Most common disabling primary headache
Chronic disorder with episodic attacks - complex changes in the brain
Normal life events can trigger or associated with migraines (stress, period, hunger, dehydration diet)
What are the symptoms of migraine?
During attacks >Headache >Nausea, photophobia, phonophobia >Functional disability In-between attacks >Enduring predisposition to future attacks >Anticipatory anxiety
What are the stages of a migraine?
Premonitory
Early headache
Advanced headache
Prodrome
What is the premonitory phase of a migraine?
Mood + cognitive changes Fatigue Muscle pain Food craving Some get an aura - 33% 15-60 minutes long normally
What is the early headache phase of a migraine?
best place to treat
Dull
Nasal congestion
Muscle pain
What is the early headache phase of a migraine?
Unilateral
Throbbing
Nausea
Photo/osma/phono phobia
What is the prodrome phase of a migraine?
Fatigue
Cognitive changes
Muscle pain
What is a chronic migraine?
Headache >=15 days/month, of which >=8 must be migraine for more than 3 months
What is a transformed migraine?
History of episodic migraine
Increasing frequency of headaches
>over weeks / months / years
>symptoms become less frequent and less severe
Some have severe migraines with daily lesser headaches
> can occur with or without escalation in medication use
In patients with medication overuse, discontinuing the overused medication often (but not always) dramatically improves headache frequency
What is a medication overuse headache?
Headache present on ≥15 days / month which has developed or worsened whilst taking regular symptomatic medication
Can occur in primary headaches
What can cause a medication overuse headache?
Migraineurs taking pain medication for another reason can develop chronic headache
Use of triptans, ergots, opiods and combination analgesics >10 days / month
Use of simple analgesics > 15 days per month
Caffeine overuse: coffee, tea, cola, irn brew
What is the abortive treatment for a migraine?
Aspirin or NSAIDs
Triptans
Limit to 10 days per month (~2 days per week) to avoid the development of medication overuse headache
What is the prophylactic treatment for a migraine?
Propranolol, Candesartan Anti-epileptics >Topiramate, Valproate, Gabapentin Tricyclic antidepressants >amitriptyline, dothiepin, nortriptyline Venlafaxine
How do you treat a migraine during pregnancy?
Avoid antiepileptics
Acute attack - use paracetoamol
Prevent with propranolol or amitriptyline
What are the causes of trigeminal autonomic cephalagias?
Cluster headache
Paraxoysmal hemicrania
SUNCT/SUNA (short lasting unliateral neuralgiform headache)
>Conjunctibital injection + tearing /autonomic symptoms
What is trigeminal autonomic cephalagias?
Unilateral head pain - very severe
Attack frequency +duration differs
Get cranial autonomic symptoms
What is a cluster headache attack?
Rapid onset + severe unilateral attacks >Mainly orbital + temporal pain - Last 15mis - 3hrs >Rapid cessation of pain Patients restless during an attack Prominent ipsilateral autonomic symptoms Migrainous symptoms often present
What are the migrainous symptoms often present in a TAC?
Premonitory symptoms: tiredness, yawning
Associated symptoms: nausea, vomiting, photophobia, phonophobia
Typical aura (often under recognised)
How can the TAC attacks present (what frequency/length)?
Either bouts that last 1-3 months or chronic clusters
Bouts
>1-8 a day
>At roughly same time each day
Chronic
>Last a year without remission
>Or remission for a month and then restart
What are the cutaneous triggers for headaches?
Wind
Cold
Touch
Chewing
What is paroxysmal hemicrania?
Excrutiatingly severe unilateral episodes with acute onset >Mainly orbital and temporal Duration: 2-30 mins Rapid cessation of pain 50% are restless and agitated during an attack Prominent ipsilateral autonomic symptoms Migrainous symptoms may be present Background cutaneous pain
What is the frequency of paroxysmal hemicrania?
2-40 attacks a day
With no circadian rhythm
What is a SUNT headache?
Unilateral orbital, supraorbital or temporal pain
Stabbing or pulsating pain
10-240 seconds duration
Cutaneous triggers
Pain is accompanied by conjunctival injection and lacrimation
What is the attack frequency for a SUNT headache?
Attack frequency from 3-200/day,
>no refractory period
What is trigeminal neuralgia?
Unilateral maxillary or mandibular division pain > ophthalmic division Stabbing pain 5 - 10 seconds duration Cutaneous triggers Autonomic features are uncommon
What is the attack frequency for tirgeminal neuralgia?
Attack frequency from 3-200/day,
>refractory period
What is the abortive treatment for a cluster headache?
Subcutaneous sumatriptan
nasal zolmatriptan
100% oxygen
What is the abortive treatment for a cluster headache bout?
Occipital depomedrone injection (same side as the headache)
Or tapering course of oral prednisone
What is the preventative treatment for a cluster headache?
Verapamil (high doses may be required)
Lithium
Methysergide (risk of retroperitoneal fibrosis)
Topiramate
What is the treatment for tirgeminal neuralgia?
No abortive treatment Prophylaxis: >Carbamazepine >Oxcarbazepine Surgical intervention can be considered (decompression)
What is the treatment for SUNCT/SUNA headaches?
No abortive treatment Prophylaxis: >Lamotrigine >Topiramate >Gabapentin >Carbamazepine / Oxcarbazepine
What presentations are more likely to have a sinister cause?
Associated head trauma First or worst Sudden (thunderclap) onset New daily persistent headache Change in headache pattern or type Returning patient
What are the main sinister headache risk factors?
Over 50 New or change in headache Focal symptoms or non-focal neurological symptoms Abnormal neurological exam Neck stiffness High/low pressure
What is a thunderclap headache?
A high intensity headache reaching maximum intensity in less than 1 minute
Majority peak instantaneously
May be primary or secondary
No reliable differentiating features!
What are the differentials of a thunderclap headache?
Primary >migraine, >primary thunderclap headache, >primary exertional headache, >primary headache associated with sexual activity Subarachnoid haemorrhage Intracerebral haemorrhage TIA / stroke Carotid / vertebral dissection Cerebral venous sinus thrombosis Meningitis / encephalitis Pituitary apoplexy Spontaneous intracranial hypotension
Who should be suspected of an SAH?
All patients presenting with a sudden severe headache that peaks within a few minutes and lasts for at least 1 hour
Examination is often normal!
Never consider a patient ‘too well’ for SAH
How do you manage a suspected SAH?
SAME DAY hospital assessment
To check for SAH
CT brain (some false negative)
LP (must be done >12hrs after headache onset)
CT +/- LP is unreliable beyond 2 weeks and angiography is required beyond this time
What are the features of a riased ICP?
Progressive headache with associated symptoms and signs
Headache is a common 1st presenting feature, but other symptoms and signs are usually present
What are the warning features of raised ICP?
Headache worse in morning or wakes patient from sleep
Headache worse lying flat or brought on by valsalva (cough, stooping, straining)
Focal symptoms or signs
Non-focal symptoms e.g. cognitive or personality change, drowsiness
Seizures
Visual obscurations and pulsatile tinnitus
What are the features of intracranial hypotension headache?
Dural CSF leak
Spontaneous or iatrogenic (post lumbar puncture)
Clear postural component to the headache
>Worsens on upright posture
>Gets better lying down
>Chronic headache often loses postural component
How do you investigate intracranial hypotension?
MRI Brain
MRI spine
How do you treat intracranial hypostension?
Bed rest Fluids Analgesia Caffeine IV caffiene if required Epidural blood patch
What is a giant cell arteritis headache?
Consider in patient over 50 with new headache
Diffuse, persistant maybe severe headache
Systemically unwell potentially
Scalp tenderness, jaw claudication + visual disturbance
Prominent temporal arteries may be present
Elevated ESR supports diagnosis
What are the eye scores for the glasgow coma scale?
Open spontaneously (4)
Open to verbal command (3)
Open to pain (2)
Does not open eyes (1)
What is the verbal scores for the glasgow coma scale?
Orientated (5) Confused speech (4) Inappropriate words (3) Incomprehensible sounds (2) No speech (1)
What is the motor response for the glasgow coma scale?
Obeys commands (6) Localises to pain (5) Normal flexion to pain (4) Abnormal flexion to pain (3) Extension to pain (2) No movement (1)
What is the pathophysiology process of haemorrhage?
Haemorrhage – ‘mass effect’
Disruption of blood brain barrier - ↑ECF (vasogenic oedema)
Membrane failure – influx of Ca – cellular swelling (cytotoxic oedema)
Influx of inflammatory mediators
>Brain swelling
>Raised ICP
What are the secondary effects of raised ICP?
Herniation syndrome
Decreased cerebral perfusion
How is cerebral blood flow regulated?
Autoregulation (myogenic) >vascular smooth muscle constricts in response to an increase in wall tension Cerebral metabolism Carbon dioxide + oxygen levels Neurohumoral factors
What are the types of herniation syndrome?
Subfalcine herniation >medial motor cortex Uncal herniation >IIIrd CN, ipsilateral corticospinal tracts Foramen magnum herniation >brain stem centres
What are the surgical interventions to reduce ICP?
Craniotomy and evacuation of clot
External ventricular drainage
Decompressive craniectomy
What are the main infections of the spinal cord?
Meningitis encephalitis cerebral abscess Post infectious encephalitis prion diseases
What is meningitis?
Inflammation or infection of meninges
What is encephalitis?
Inflammation or infection of Brain substance
What is myelitis?
Inflammation or infection of spinal-cord
What are the differentials of meningitis?
Infective: bacterial, viral, fungal
inflammatory: sarcoidosis
drug induced: NSAIDs, IVIG
malignant: metastatic, haematological
What are the clinical features of encephalitis?
Flulike prodrome progressive headache associated with fever +/- meningism progressive cerebral dysfunction >confusion >abnormal behaviour >memory disturbance >depressed conscious level >seizures line focal symptoms/signs
What are the antibodies that cause autoimmune encephalitis?
Anti-VGKC (voltage-gated potassium channel)
anti – NMDA receptor
What are the symptoms of anti – NMDA receptor encephalitis?
flu like prodrome
prominent psychiatric features
altered mental state and seizures
progressing to a movement disorder and coma
What are the symptoms of Anti-VGKC (voltage-gated potassium channel) encephalitis?
results in frequent seizures
amnesia
altered mental state
How do you investigate encephalitis?
blood cultures
imaging (CT scan +/- MRI)
lumbar puncture
EEG
What are the contraindications to lumbar puncture?
vocal symptoms or signs – suggest focal brain mass
reduce conscious level – suggest raised intracranial pressure
new onset seizures
papilloedema
severe immunocompromised state
What are enteroviruses?
A large family of RNA viruses with a tendency to cause CNS infections
spread by faecal oral route
many cause non-paralytic meningitis
do not cause gastroenteritis
include polio viruses Coxsackieviruses and echo viruses
What are arboviruses?
Common other parts the world
transmitted to man by vector (mosquito) from nonhuman host
Called Arbo as arthropod borne
relevant to travel (travel history important some preventable by immunisation)
What is a brain abscess?
localised area of pus within brain
what is sub dural empyema
thin layer of pus between Dura and arachnoid membranes over surface of brain
Were the clinical features of the brain abscess
fever, headache
physical symptoms/signs – seizures, dysphasia, hemi paresis
signs of raised intracranial pressure – depressed conscious level, papilloedema, false localising signs
meninges may be present particularly with empyema
features of underlying source – dental, sinus or ear infection
What are the causes of brain abscess/empyema?
any focal lesion but most commonly tumour, subdural haematoma penetrating head injury grateful adjacent infection blood-borne infection neurosurgical procedure
How do you diagnose a brain abscess/empyema?
imaging CT or MRI
investigate source
blood culture
biopsy
How do you manage a brain abscess?
surgical drainage of possible
penicillin or ceftriaxone to cover streps
Metronidazole for anaerobes
high doses required for penetration
culture and sensitivity tests on aspirate provide useful guide
high mortality without appropriate treatment
What are the spirochaetes infections of the CNS?
Lyme disease (Borrelia burgorferi) syphilis (Treponema pallidum) leptospirosis (Leptospira interrogans)
What is lyme disease?
vectorborne tick in wooded areas
caused by Borrelia burgdorferi
3 stages
multisystem – skin, rhuematological, neurological, cardiac and ophthalmological involvement
What is the first stage of lyme disease?
early localised infection
characteristic expanding Russian state of tick bite: arrhythmia migrans
50% flulike symptoms in days to one week
What is the second stage of lyme disease?
early disseminated infection weeks to months
1 or more organ systems involved
muskets greater neurological involvement most common
What is the third stage of lyme disease?
chronic infection months to years occurring after period of latency
What are the types of neurological involmenet in lyme disease?
Mononeuropathy mononeuritis multiplex painful radiculoneuropathy cranial neuropathy myelitis Meningo-encephalitis subacute encephalopathy encephalomyelitis
How do you investigate lyme disease?
complex range of serological tests CSF lymphocytosis PCR of CSF MRI brain/spine CMS involvement brain conduction studies/EMG if PNS involvement
How do you treat lyme disease?
prolonged antibiotic treatment –
>IV ceftriaxone,
>oral doxycycline
What is neuro syphillis?
Causative agent Treponema pallidum
3 stage presentation primary, secondary, latent
Tertiary disease years or decades after primary disease – not common
Treated with high dose penicillin
What is poliomyelitis?
caused by polio virus types 1 and 2 or 3 – all enteroviruses
paralytic disease in 1% rest asymptomatic
asymmetric flaccid paralysis especially in legs
no sensory features
polio immunisation contains all 3 poliovirus types
>Changed to oral after 2004
What is Rabies?
an acute infectious disease of CNS affecting almost all mammals
transmitted to humans by bite or slavery contamination of open lesion
neurotrophic – virus and his peripheral nerves and migrate to CNS
paraesthesia at site of original lesion
What is tetanus?
infection with Clostridium tetani – anaerobic gram-positive bacilli
wound may not be apparent
acts at neurological junctions; blocks inhibition of motor neurons
results in rigidity and (risus sardonicus)
How do you prevent tetanus?
immunisation (toxoid)
given combined with other antigens (DTaP)
penicillin and immunoglobulin for high risk wounds/patients
What is botulism?
causative agent Clostridium botulinum
an anaerobic spore producing gram-positive bacilli produces neurotoxin
binds irreversibly to pre-synaptic membranes of peripheral neuromuscular and autonomic nerve junctions
>toxin binding blocks ACH release
>recovery both sprouting new axons
motor infection, infantile (intestinal colonisation), foodborne, wound (almost exclusively injecting or popping drug users)
How does botulism present?
incubation period 4 to 14 days
descending symmetrical flaccid paralysis
Julie motor, respiratory failure, autonomic dysfunction (usually pupil dilation)
How do you diagnose botulism?
nerve conduction studies, mouse neutralisation bioassy for toxin and blood
culture from the provided wound
How do you treat botulism?
antitoxin (A, B, E)
penicillin/Metronidazole (prolonged treatment)
radical wound debridement
What is post-infective inflammatory syndrome?
proceeding infection (viral, bacterial) or immunisation latent interval between precipitating infection and onset of neurological
What are the symptoms of post-infective inflammatory syndrome?
autoimmune Central nervous system >acute disseminated encephalomyelitis my latest peripheral nervous system >Gillian Barre syndrome (GBS)
What are the clinical features of Jakob disease CJD?
insidious onset (usually Auden 60) early behavioural abnormalities rapidly progressive dementia myoclonus progression to global neurological decline motor abnormalities – cerebellar ataxia, extra pyramidial, pyramidial cortical blindness seizures may occur
What are the differential diagnoses of CJD
Alzheimer’s disease is myoclonus – usually more prolonged
subacute sclerosing panencephalitis– very rare chronic infection with defective measles virus
CNS vasculitis
inflammatory encephalitis
What is the prognosis of CJD?
rapid progression, death often within 6 months
What is new variant CJD?
Young onset less than 40
linked to bovine spongiform encephalopathy in cattle
eating infected material, less cases than predicted
new cases last few years
early behavioural changes more comments
longer course (average 13 months)
How do you investigate CJD?
MRI
EEG
CSF
