headache Flashcards
the CNS is derived from what embryonic layer?
ectoderm
during early development of the CNS 3 primary vesicles arise then 5 secondary vesicles -forebrain (telencephalon and diencephalon), midbrain (mesencephalon) and hindbrain (metencephalon and myelencephalon) - what are the adult derivatives of these secondary structures?
telencephalon:
= cerebral hemispheres with later ventricles
diencephalon:
= thalamus and 3rd ventricle
mesencephalon:
= midbrain and cerebral aqueduct
metencephalon:
=pons, cerebellum and 4th ventricle
myelencephalon:
= medulla and 4th ventricle
what layer does nerve cell migration start and finish?
ventricular zone to cortex
what cells do nerve utilize for migration. what condition arises if this transport system doesn’t work?
radioglial cells
epilepsy
what cell is responsible for myelinating neurons in the CNS and PNS, how do they differ?
CNS = oligodendrocytes
PNS = Schwann cells
*oligodendrocytes secrete myelin sheaths around many neurons. Schwann cells wrap their cell body around each neuron separately
T or F. A brainstem lesion will usually produce ipsilateral cranial nerve defect
True
*exception = trochlear nerve: axons cross in midline
what CNs arise from the midbrain, pons and medulla?
midbrain = oculomotor and trochlear
pons = trigeminal, abducens, facial, vestibulocochlear
medulla = glossopharyngeal, vagus, accessory and hypoglossal
what condition is caused by damage to the sympathetic innervation to the face?
a brainstem lesion will produce an ipsilateral Horner’s syndrome: miosis, ptosis, and anhidrosis (absence of sweating of the face)
what ascending (sensory) white matter tract is responsible for pain, temperature, touch and pressure? where do fibres cross and what is the consequence of this?
spinothalamic tract, decussates early so are susceptible to central cord pathology
what ascending (sensory) white matter tract is responsible for touch vibration and proprioception? where does it cross?
dorsal column-medial lemniscal pathway. crosses in the medulla
why is the pathway for light touch sensation unique?
Not specific to one pathway. it travels with both the spinothalamic tract and the dorsal column-medial lemniscal tract
what conditions may affect the dorsal spinal cord?
- vitamin B12 deficiency (subacute combined degeneration of the spinal cord)
- MS
- HIV myelopathy
there are two columns in the dorsal-column medial lemniscus pathway that transmit information from the upper and lower limbs. what are they?
the cuneate column transmits information from the upper limb, neck and trunk.
the gracilis column transmits information from the lower limbs
what pathway is ipsilateral and controls coordination?
spinocerebellar tract
unconscious proprioception
what major descending (motor) white matter tract is responsible for movement by innervating skeletal muscles? where does it cross?
corticospinal tract. crosses in the medulla (ventral pyramids)
what is the difference between a pre-motor lesion and a primary motor area lesion?
if the primary motor cortex is destroyed you have a complete weakness and hemiplesia
if the premotor area is destroyed (controls higher functions of movement) you get apraxia - difficulty with motor planning
the motor system as a whole integrates information from different modalities, in the parietal cortex, to focus attention on relevant target and/or upon the spatial relationships of objects. what are these modalities?
- somatic sensory area (about limb position)
- vestibular system (about head position)
- premotor areas (about motor plans)
- visual system
- limbic cortex (about motivational state
what are the 3 major sources of input into the corticospinal tract that fine tune movement?
- sensory receptors
- cerebellum
- basal ganglia
compare and contrast upper and lower motor neuron lesions?
UMN vs LMN:
- weakness = present both (UMN: arm extensors and led flexors)
- atrophy = absent vs present
- reflexes = increased vs decreased
- tone = increased vs decreased
- fasciculations = absent vs present
- Babinski (extension of toes) = present vs absent
where is CSF produced, what is its pathway and where is it reabsorbed?
- produced by choroid plexus in lateral ventricles
- travels down 3rd ventricle -> cerebral aqueduct -> 4th ventricle -> spinal cord or surround brain (via foramen of Luschka or foramen of Magende
- reabsorbed in arachnoid granulations in venous sinuses (drain brain into internal jugular veins)
what would you expect to see in CSF from lumbar puncture?
- virtually no proteins <0.5mg/ml
- no RBC
- <5 WBC/m
- glucose 60-70% blood levels (2.5-5mmol)
when should you never carry out/ what are the contraindications of LP?
**if there is any possibility of space occupying lesion!! (risk of coning)
- cardiorespiratory instability
- focal neurological signs
- signs of ICP (coma, high BP, low HR or papilloedema)
- coagulopathy
- local infection at site of LP
what is the normal opening pressure of CSF and when is it considered elevated?
<20cm water, elevated >30cm
what happens if CSF flow is blocked (congenital aqueduct stenosis, infection, inflammation, tumours, idiopathic intracranial hypertension etc.)?
- fontanelle unfused = hydrocephalus with expanded cranium
- fontanelle fused = can be normal if occurs slowly, but if fast can cause ICP, drowsiness and coma
what are the features of a low pressure headache?
- eased on lying down, worse standing up
- can occur spontaneously, but usually post LP
clinical presentation of meningitis - inflammation of the meninges
- stiff neck
- petechial rash (non-blanching), progressive is suggestive of meningococcal infection
- bulging fontanelle
- photophobia
- fever
- headache (severe + generalised)
- altered mental state (confusion/lethargy)
- +ve brudzinski and kernig sign
investigation of meningitis
LP:
- bacterial= glucose low, protein raised, neutrophils raised, cloudy
- viral= glucose normal, raised proteins, lymphocytes raised, clear
CT if suspect contraindications of LP
FBC:
-shows infection, but not where
coagulation screen:
-check can clot okay
Management of meningitis
- ABC
- haemodynamically stable (e.g. shock = hypotension)
- fluid balance
- electrolyte balance
- start antibiotics -> CEFOTAXIME IV 2g immediately 12-hourly (if pt >50 y/o, pregnant, immunocompromised or on steroids, add amoxicillin 2g every 6 hours to provide Listeria cover)
- steroid - dexamethasone 0.15g/kg 6-hourly
-prophylaxes family with ciprofloxacin
Clinical presentation of brain abscess - focal, intracerebral infection evolving from an area of cerebritis into a collection of purulent material enveloped in a vascularized capsule
*caused by direct or indirect spread from infection in paranasal sinuses, middle ear and teeth
- vomiting
- bulging fontanelle
- increased head circumference
- separation of sutures
- hemiparesis
- focal seizures
- increased WBC count
- can occur with neonatal meningitis
investigation of brain abscess
- CBC: raised WBC!
- serum erythrocyte sedimentation rate (ESR): elevated
- MRI/CT
management of brain abscess
(broad spectrum)Cefotaxime IV 2-4g 8-hourly + metronidazole IV 500mg 8-hourly
drainage of abscess
clinical presentation of encephalitis - inflammation of the brain
-altered mental state (encephalopathy-altered state of consciousness, seizures, personality changes, cranial nerve palsies, speech problems, and motor and sensory deficits) and FEVER!
what type of infection causes lab findings of the following in CSF analysis:
a) gram-negative diplococci?
b) gram-positive diplococci?
c) gram-negative coccobacilli?
d) gram-positive rods and coccobacilli?
a) Neisseria meningitidis
b) Streptococcus pneumoniae
c) Haemophilus influenza
d) Listeria
what organisms are most likely to cause bacterial meningitis - depending on age?
neonates:
- E.coli
- group B strep
- listeria
<5yrs:
-N. meningitidis
young adults:
-N. meningitidis
older:
- S.pneumoniae
- listeria
immunosuppressed:
- M.tuberculosis
- Cryptococcus
shunt:
-staph aureus
what organisms are most likely cause viral meningitis?
- enterovirus
- mumps
- herpes simplex
what type of infection causes lab findings of the following in CSF analysis:
a) gram-negative diplococci?
b) gram-positive diplococci?
c) gram-negative coccobacilli?
d) gram-positive rods and coccobacilli?
a) Neisseria meningitidis
b) Streptococcus pneumoniae
c) Haemophilus influenza
d) Listeria
what type of infection causes lab findings of the following in CSF analysis:
a) gram-negative diplococci?
b) gram-positive diplococci?
c) gram-negative coccobacilli?
d) gram-positive rods and coccobacilli?
a) Neisseria meningitidis
b) Streptococcus pneumoniae
c) Haemophilus influenza
d) Listeria
what type of infection causes lab findings of the following in CSF analysis:
a) gram-negative diplococci?
b) gram-positive diplococci?
c) gram-negative coccobacilli?
d) gram-positive rods and coccobacilli?
a) Neisseria meningitidis
b) Streptococcus pneumoniae
c) Haemophilus influenza
d) Listeria
what are the most common viral causes of encephalitis (rarely bacterial)?
- herpes simplex!! (most common)
- arboviruses
- mumps
- measles
investigations of encephalitis?
- CT head or MRI (brain imaging): demonstration of temporal lobe oedema
- LP: clear, increased WBC count, normal glucose, protein + herpes simplex virus identified through PCR.
management of encephalitis
- medical emergency therefore ABC
- supportive Rx
- corticosteroid if ICP
- antiviral therapies = ACICLOVIR until cause determined
what is the treatment for tension headache?
- reassurance (wont go away overnight)
- explain muscles around head
- reduce analgesics as this can contribute the headache
- relaxation exercises
- low dose amitriptyline
what is the acute treatment of migraine?
first-line:
- ASPRIN (900mg) and if nausea give anti-nausea
- Triptans (sumatriptan); 5HT-1d receptor agonists
what prophylaxis treatment can be given to frequent migraine suffers?
- first-line = beta blockers - propranolol (avoid in asthmatics)
- topiramate
- low dose amitriptyline
- candesartan
- sodium valproate (risk of foetal malformation)
- botulinum toxin
what is the treatment of trigeminal autonomic cephalgia (TAC) conditions like cluster headaches o paroxysmal hemicranias?
- high flow oxygen
- triptan
- high does verapamil (CCB)
- indomethacin (NSAID) in paroxysmal hemicrania
my definition what time period would someone have medication overuse headache?
present for >15 days/month
CT head is requested first in query thunderclap headache (severe and rapid onset headache!). what investigation usually follows after 6hrs?
LP, look for bilirubin and oxyhaemoglobin -> subarachnoid haemorrhage
what are the signs and treatment of raised intracranial pressure?
- SERIOUS
- mild headache
- diurnal variation
- worse in mornings
- mild nausea
- neurological features
- papilledema
*urgent referral and scan (tumour, abscess or CSF blockage)
what is used to treat temporal arteritis and why is prompt treatment important?
steroids quickly as risk of blindness
what is cerebral venous sinus thrombosis?
thrombosis in the cerebral veins (draining the brain). often in females on OCP, sever headache and seizures. usually bilateral on MRI. treat with clot busting drugs and referral
how can you treat low ICP?
usually as a cause of LP therefore use blood patch
what are the non tumour causes of early morning headaches?
- neck degeneration, pressure on intervertebral joints (inflammation and arthritic, with muscle spasm): wont have neurological issues
- sleep apnoea
- obesity
what are the two different types of sleep and how are the distinguished?
- slow wave sleep
- REM sleep
distinguished using EEG
what is an EEG?
- electroencephalogram
- records brain activity
- main use is to detect and investigate epilepsy
- small blunt sensors attached to scalp
- beta waves when awake and eyes open
- alpha waves when awake but eyes closed/resting
- theta waves when sleeping
- delta waves when in deep sleep (appear stage 3)
what stage of sleep do you get K complexes and sleep spindles?
stage 2
what is associated with REM sleep?
- rapid eye movements
- increase in HR
- increased neural activity
- increase in respiration and oxygen consumption
- associated with penile erection
- dreaming occurs
- body temp drops
- movement inhibited
what is associated with slow wave sleep?
State 3 red flags that indicate raised intracranial pressure.
- Headache worse when sneezing/coughing.
- Worse bending down or lifting
- Worse first thing in the morning
State 2 red flags that you may gather from a patient’s history that may indicate a space-occupying lesion.
- Seizures
- Change in behaviour/personality
Name causes of raised intracranial pressure.
- Congenital
- Acquired
- Idiopathic (common in obese females: the main treatment is weight loss, but can use diuretics too)
How would you differentiate between idiopathic intracranial hypertension and a brain tumour headache?
IIH: double vision, temporary loss of vision, works in the morning, and on coughing/sneezing
Brain Tumour: Seizures, mental/behavioural changes, progressive weaknesss, paralysis, vision/speech problems
State the primary functions of the following brain lobes:
1- Frontal 2- Temporal 3- Parietal (R) 4- Parietal (L) 5- Occipital
1- Frontal = Speech and Language 2- Temporal = Memory 3- Pareital (R) = Special Senses 4- Pareital (L) = Language 5- Occipital = Vision
State an important contraindication of sodium valporate (Anti-epileptic)
Pregnancy
State the pathophysiology of narcolepsy (inappropriate day time sleepiness). (unlikely we need to know as not part of the learning outcomes)
- Autoimmune (linked to chromosome 6)
- Loss of orexin neurons in the lateral hypothalamus
(Orexinergic neurons usually excite arousal centres in the lateral hypothalamus which produce 5HT, NA, AcH etc… which inhibit the sleep centre in the brain (VLPO) and cause wakefulness, so when these are damaged the person feels sleepy all the time)
Define epilepsy.
The tendency to have seizures due to sudden discharges of abnormal electrical activity.
Informative question - Why do we need to know the types of seizures and be able to classify them?
Important for treatment
Some drugs may make certain seizures worse!
How would you diagnose epilepsy?
1- History
2- Investigations: ECG, EEG, MRI
List the main categories of epilepsy.
- Partial Seizures (Simple or Complex partial seizures) which evolve into secondary generalised seizures
- Generalised Seizures
- Unclassified epileptic seizures
A) State what is meant by a partial seizure.
B) Briefly Describe the two categories of partial seizures.
A) Seizures where the electrical activity is localised to one hemisphere or lobe in the brain (they physical and emotional effects, you feel/see/hear things)
B)
Simple partial seizure:
- Focal with minimal spread of abnormal discharge
- remains conscious and aware
- experience strange sensation (smell, taste) with some jerking movements
Complex partial seizure:
- Local onset then spreads (clinical symptoms depend on the amount of spread, so the aura or motor activity that they might experience)
- impaired consciousness (the person may not remember what happened during the seizure)
In which lobe is complex partial seizures most common?
Temporal lobe.
What is a secondary seizure?
- One that starts partially then becomes generalised.
- Different durations, stiffness and jerking phases
- followed postictal confusion and somnolence (sleepiness)
A) What is a generalised seizure?
- Affects both hemispheres of the brain
- Impaired consciousness
- 1-3 minutes
List different types of generalised seizures.
- Tonic: Stiffness of muscles (in legs, arms, and neck tense up and if you are standing you can fall)
- Atonic: muscles go limp, the patient may fall forwards
- Clonic: jerking due to muscle spasms/convulsions
- Tonic-Clonic: tonic followed by clonic (most common type)
- Myoclonic: short muscle twitching (see in a variety of seizures)
- Absence: Sudden loss and abrupt regaining of consciousness (“spaced out”), the attack may be associated with some clonic jerking of the eyelids or extremities, postural tone change.
A) Define Status Epilepticus.
B) State how you would treat this condition.
A) Any seizure that lasts more than 5 minutes or repetitive seizures without regaining consciousness. A life-threatening condition.
B) Medical Emergency (call 911 unless you know the person o usually have seizures that last that long): Use Benzodiazepines (to enhance GABA)
(Informative Question)
Describe the cellular mechanisms of seizure generation.
- EPSPs (Excitory Postsynaptic Potential
- Na+ Influx
- Ca++ currents
- Paroxysmal depolarisation
State the target of an Anti-epileptic drug.
- Increase inhibitory neurotransmitter system (GABA)
- Decrease excitatory neurotransmitter system (Glutamate)
- Block the voltage-gated inward positive current of Na+ or Ca 2+
- Increase positive outward current (k+)
Where are the excitatory neurotransmitters glutamate and acetylcholine found?
Glutamate = CVS Acetylcholine = PNS
Name commonly used epilepsy drugs + indications + side effects + prominent contraindications.
1- Sodium valproate (increases GABA in CNS) - general seizures - hair loss - AVOID IN PREGNANCY
2- Carbamazepine (inhibition of Na+ channels at high firing frequency) - partial seizures + secondary generalised - strong sedative eside effect - WILL AFFECT CONTRACEPTIVE FUNCTION
3- Lamotrigine (Inhibition of Na+ channels) - good for al seizures - SKIN RASH
4- Oxcarbazepine - same as carbamazepine but better tolerated
Which drugs are the first line of treatment of status epilepticus?
- Lorazapam (laura is za bomb!) and diazepam (Dia is za the bomb!)
