Neurology Flashcards
What is a migraine characterised by?
- a severe, unilateral, throbbing headache
- associated with nausea, photophobia and phonophobia
- attacks may last up to 72 hours
- patients characteristically go to a quiet, dark room during an attack.
classic migraine attacks are precipitated by an aura. - typical aura are visual, progressive and last 5-60 minutes, transient hemianopia disturbances
what are the risk factors for migraines and triggers for migraines?
Risk Factors
- Family history
- high caffeine intake
- exposure to change in barometric pressure
- females
Triggers
- tiredness, stress
- alcohol
- COCP
- lack of food/dehydration
- cheese, chocolate, red wines, citrus fruits
- menstruation
- bright lights
what are the diagnostic features for migraine?
- presence of risk factors
- prolonged headache
- nausea
decreased ability to function - if the headache has the following characteristis - unilateral location, pulsating quality, moderate to severe pain intensity, aggravation by or causing avoidance of routine physical activity
- if it is not attributed to anything else
what investigations would you consider for migraines?
it is a clinical diagnosis
consider
ESR, LP, CSF, CT head
how do you treat migraines?
Rescue therapy - sumatriptan and high flow oxygen.
to treat mild to moderate symptoms
- give NSAIDs or aspirin
you can add anti-emetics
2nd line = paracetamol mono-therapy
to treat severe symptoms
1st line -triptan (almotriptan)
you can add anti-emetic, hydration and NSAIDs
2nd line - ergot alkaloids (ergotamine/caffine)
Prophylaxsis
- propranolol is 1st line
- topiromate can be given if BB is not suitable
what is a tension headache?
a form of primary headache
they can episodic or chronic
they are rarely disabling
what are the characteristic features of a tension headache?
often described s a tight band around the head or a pressure sensation - symptoms tend to be bilateral (migraine tend to be unilateral)
lower intensity than a migraine
not associated with aura, nausea/vomiting o aggravated by routine physical activity
may be related to stress
what is a chronic tension headache defined as?
tension headache lasting more than 15 days per month
how would you treat acute and chronic tension headaches?
acute - simple analgesics (aspirin, paracetamol, ibuprofen, naproxen)
Chronic symptoms - antidepressants (amitriptyline or doxepin)
what are the features of a cluster headache?
attacks of severe pain localised to the unilateral orbital, supra-orbital, and/or temporal areas; they last 15 minutes to 3 hours.
the attacks usually occur at the same time period for several weeks
they can occur from once every other day to 8 times per day
may be accompanied by redness, lacrimation, lid swelling.
more common in men and smokers
what investigations would you order for cluster headaches?>
Brain CT or MRT - to eliminate secondary causes
ESR - exclude giant cell arteritis in patients over 50
pituitary function tests - to exclude secondary causes
how do you treat an acute attack of cluster headache?
1st line
- subcutaneous sumatriptan with high flow oxygen
2nd line
- intranasal zolmitriptan (nasal)
- if they have CVD of uncontrolled hypertension then the first line should be just oxygen
how do you treat ongoing episodic/chronic cluster headache?
1st line - verapamil
2nd line - lithium, topiramate, gabapentin or melatonin
what are the tiggers for cluster headaches?
alcohol
volatile smells
warm temps
sleep
what is temporal arteritis?
a large vessel vasculitis
It primarily affects branches of the external carotid artery and is the most common form of vasculitis in adults.
Typically occurs in woman older than 50.
what are the clinical features of temporal arteritis?
typically older than 50
usually rapid onset (less than one month)
headache
jaw claudication
visual disturbances secondary to anterior ishcemic optic neuropathy - can be transient or visual loss
tender, palpable temporal artery
around 50% will have features of polymyalgia rheumatica (aching, morning stiffness in proximal limb muscles)
also there may be lethary, depression, low grade fever, anorexia, night sweats.
what are the investigations for temporal arteritis?
ESR
CRP
FBC
LFTs
consider temporal artery biopsy (will show skip lesions)
aortic arch angiography
how do you treat suspected and confirmed temporal arteritis?
suspected with no visual/neurological symptoms - prednisolone
suspected with neurological symptoms or signs - methylprednisolone plus IV pulse therapy
confirmed temporal arteritis
1st line prednisolone and aspirin can be added plus osteoporosis prevention (calcium carbonate and ergocalciferol and alendronic acid)
what are some differential diagnosis for acute single episode headaches?
meningitis encephalitis subarachnoid haemorrhage head injury sinusitis glaucoma tropical illness
what is an ischaemic stroke?
when blood supply in a cerebral vascular territory is critically reduced due to occlusion or stenosis of a cerebral artery.
Symptoms must last for more than 24 hours
what is a transient ischaemic attack?
it has typical symptoms of rapidly resolving unilateral weakness or numbness
what is a haemorrhagic stroke?
vascular rupture with bleeding into the brain parenchyma
what are the types of ischaemic strokes?
thrombotic (thrombosis from large vessels e.g. the carotid) Embolic stroke (usually a blood clot but fat, air or clumps of bacteria can also act as an embolus. Also AF is an important cause of emboli forming in the heart)
what are the risk factors for an ischaemic stroke?
general RF for CV disease - age, hypertension, smoking, hyperlipidaemia, DM)
Fam history
AF
what are the key diagnostic features of a stroke?
vision lost or visual field deficit (homonymous hemianopia) weakness aphasia impaired co-ordination swallowing problems
what are the first line investigations to order for a stroke?
1st line - CT head,
MRI brain,
serum glucose and serum electrolytes (hypoglycaemia and electrolyte imbalances may cause focal neurological symptoms),
serum urea and creatinine (renal failure may be a potential contraindication for some stoke treatment),
ECG to exclude cardiac arrhythmia or ischaemia,
FBC to detect conditions that may be potential contraindications for some acute stoke treatment and interventions,
prothrombin time and PTT
what would you see on CT and MRI of a person who has had an ischaemic stroke?
in many cases - the CT is normal within the first few hours of an ischaemic stroke
You would see hypo-attenuation (darkness) or the brain parenchyma; loss of grey matter- white matter differentiation and sulcal effacement; hyper-attenuation (brightness) in an artery indicated a clot)
MRI - contraindicated in patients with certain metal implants such as pacemakers
acute ischaemic infarct appears bright on diffusion-weighted imaging
how do you treat an ischaemic stroke?
presentation within 4.5 and no contraindication to thrombolysis
1st line = alteplase
aspirin can be added, or endovascular intervention
Plus supportive care and swallowing assessment
for non-ambulatory patients give VTE propyhlaxis (heparin)
presentation after four hours or contraindication to thrombolysis
aspirin and supportive care
swallowing assessment
add VTE prophylaxis (heparin)
what are the clinical features of a TIA?
symptoms last less than 24 hours but typically resolve within one hour
focal neurological deficit - unilateral weakness or sensory loss, amaurosis fugax or hemianopsia, aphasia, cranial nerve defects, vertigo, lack of coordination, ataxi, syncope.
risk factors for TIA
AF valvular disease carotid stenosis congestive heart failure hypertension DM smoking alcohol abuse advanced age
what is ABCD2
for TIA - risk of stroke after a TIA age over 60 BP over 140/90 clinical features (unilateral weakness or speech impairment) duration of symptoms diabetes
how is a TIA treated?
atherosclerotic or small-vessel TIA - 1st line - platelet therapy (aspirin or aspirin plus clopidogrel) plus a lipid lowering agent (atorvastatin)
if there is greater than 50% carotid stenosis - stent
If there is a cardioembolic TIA without ischaemic heart disease give anticoagulation (warfarin or rivaroxaban) as first line
If there is TIA with ischaemic heart disease - anticoagulation plus lipid lowering agent
what investigations would you order for a TIA?
blood glucose - hypoglycaemic events can mimic TIA
chemistry profile - sever hyponatraemia can trigger seizures or induce generalised weakness
extremely low potassium or very high calcium can also cause generalised weakness
FBC
prothrombin time, INR and activated PTT
ECG
brain MRI with diffusion
fasting lipid profile
what are the different types of haemorrhagic strokes?
intraparenchymal/intracerebral bleeding within the brain)
subarachnoid (bleeding on the surface of the brain)
intraventricular
what are the risk factors for haemorrhagic stoke?
age hypertension arteriovenous malformation anticoagulation therapy male sex asian, black and/or hispanic
what are the key features of a haemorrhagic stroke?
altered sensation headache weakness sensory loss aphasia dysarthria ataxia
Headache Altered mental status Nausea & Vomiting Hypertension Seizures Focal neurological deficits
what are some features of headaches which suggest subarachnoid or intracerebral?
intracerebral - usually insidious onset and gradually increasing intensity
Sudden onset with gradual moderation or the most severe headache of my life - suggests subarachnoid
thunderclap headache is characteristic88 of subarachnoid headache.
what investigations would you perform for a suspected haemorrhagic stroke?
None infused CT - will show hyperdense lesion
chemistry panal
FBC - to exclude thrombocytopenia asa cause of haemorrhage, also a low platelet count suggests a secondary cause of haemorrhage
clotting factors to rule out coagulopathy
ECG
platelet function test
urine drug screen
LFT
ICH score
how do you treat a haemorhagic stroke?
1st line -neurosurgical evaluation
airway protection and aspiration precautions
support
what is cerebellar syndrome?
a disorder when the cerebellum becomes inflamed or damaged.
the cerebellum is the area of the brain responsible for controlling gait and muscle coordination.
what are the symptoms of cerebellar disease?
DANISH Dysdiadochokinesia, Dymetria (past pointing) A ataxia N nystamus I intention tremour S- slurred staccato speach H- Hypotonia
what are the causes of cerebellar syndrome?
stoke alchohol MS hypothyroidism drugs - phenytoin, lead poisoning, paraneoplastic e.g. secondary to lung cancer
what is status epilepticus?
5 or more minutes of either continuous seizure activity or repetitive seizures without regaining consciousness
what are generalised seizures
generalised tonic-colonic seizures classically involve loss of consciousness and a phasic tonic stiffening of the limbs, followed by repetitive clonic jerking.
what are absence seizures?
characterised by abrupt cessation of activity and responsiveness, minimal associated movements, staring episodes, and no aura/postical state
what is a focal seizure?
previously termed partial seizure
clinical manifestations of seizures that arise from one portion of the brain.
the level of awareness can vary
can be motor or non-motor
what investigations would order for generalised seizures?
EEG
blood glucose
FBC - look for infection
electrolyte panel
toxicology screen - illicit substances may cause seizures
head CT - may reveal a structural lesion
serum prolactin - greater than twice the baseline indicated GTCS
serum creatine kinase
how are acute generalised seizures managed?
1st line - IV or rectal benzodiazepine (lorazepam) plus supportive care
what is the ongoing treatment for generalised seizures?
1st line sodium valproate
other primary options include lamotrigine, topiramte, oxcarbazepine, carbamazepin, phenytoin.
secondary options include - zonisamide, lacosamide, clobazam, gabapentin
if monotherapy does not work anticonvulsant duel therapy can be used
lamotrigine and topiramate
lamotrigine and valproic acid
topiramate and carbamezapine
what are the features of a focal seizure?
movement of one side of the body or one specific body part
a premonitory sensation or experience (fear, epigastric sensation, deja vu)
automatisms (picking at clothes, smacking of lips)
temporary aphasia
staring and loss of contact with the environment
what are the investigations for focal seizures?
blood glucose FBC electrolyte panal toxicology screen LP and CSF analysis CT head MRI brain EEG
what is the management of multiple focal seizures in a short interval?
1st line - lorazepam/diazepam plus airway maintenance
what is the first line treatment for ongoing focal seizures?
carbamazepine
other anti-epileptics can also be used
what investigations should be ordered for absence seizures?
EEG
how are absence seizures managed?
if no history of GTCS
1st line - ethosuximide or valproic acid or lamotrigine
2nd line - topiramate or zonisamide or levetiracetam
If there is a history of GTCS
valproic acid or lamotrigine
what is non-epileptic attack disorder?
epileptic seizures that are not caused by electrical activity in the brain
what are the clinical features of non-epileptic attack disorder?
most common they will mimic tonic colonic seizure
the person does not usually loose consciousness but they may be unable to respond or react during the attack
some may have an aura
what causes non-epileptic attack disorder?
it is currently believed that it is the brain’s response to overwhelming stress or when the brain has overload
often people with this disorder have other health problems such as chronic illness, anxiety or depression
how is non-epileptic attack disorder diagnosed?
EEG - measures electrical activity in the brain
a raised prolactin suggests epileptic seizure
what is narcolepsy?
a chronic condition characterised by a disruption of the sleep-wake cycle and rapid eye movement (REM) sleep intrusion.
They can not regulate wake-sleep cycles
what are the symptoms of narcolepsy?
excessive day time sleepiness
cataplexy (sudden and transient loss of muscle tone caused by strong emotion)
hypnagogic/hypnopompic hallucinations as(as waking or as falling to sleep)
sleep paralysis
only 10-15% of people will have all 4 symptoms
what investigations would you perform for narcolepsy?
actigraphy and sleep diary
overnight polysomnography
mulstiple sleep latency test
how do you treat narcolepsy?
sleep hygiene and lifestyle changes
- patients should be advised to sleep at regular times, to avoid shift work, have 15-30 min naps at lunchtime and/or afternoon
patients should avoid heavy meals and afternoon caffeinated beverages and should abstain from alcohol
adequate psychosocial support should be given
plus - Modafinil
how do you treat narcolepsy with cataplexy?
1st line - avoidance of trigger plus sodium oxybate and/or antidepressants (fluoxetine, venlafaxine)
2nd line - monoamine oxidase inhibitors (MAOIs)
what is shingles?
shingles (herpes zoster) is an acute, unilateral, painful blistering caused by reactivation of the varicella zoster virus
what are the symptoms of shingles?
localised pain to a dermatome, the pain is burning, stinging, itching or tingling and ranges from mild to severe) - the most commonly involved ganglia are the thoracic and trigeminal nerves
pruritus in the affected dermatome
rash - erythematous maculopapular rash, which is followed by the appearance of clear vesicles. The vesicle eventually pustulate and form crusts
if the trigeminal nerve is affected the rash may cause corneal ulceration.
how is shingles managed?
oral antiviral therapy (famciclovir, secondary option is aciclovir)
plus simple analgesics plus calamine lotion
if severe pain give opioid analgesics and topical analgesics
if there is eye involvement - prompt referral to the ophthalmologist
what are the complications of shingles?
herpes zoster opthalmicus - if it occurs in the trigeminal nerve - the infection may cause conjunctivitis, keratitis, corneal ulceration, glaucoma and blindness.
superinfection skin lesions (staph or strept)
encephalitis
transverse myelitis
varicella zoster retinitis
disseminated zoster - seen in severely immunocompromised patients, the vesicular rash involves several dermatomes and visceral involvement may also occur (IV aciclovir should be used)
who is the shingles vaccine given to?
offered to all patients aged 70-79
is is contraindicated in immunocompromised patients
what causes wernicke-korsakoff syndrome?
caused by deficiency of thiamine
what is wernicke’s encephalopathy?
a neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestation
why does thiamine deficiency cause problems?
because thiamine deficiency causes impaired glucose metabolism and decreases cellular energy
the brain is vulnerable to impaired glucose metabolism
this leads to neuronal death in certain neuronal populations with high metabolic requirements and high thiamine turnover.
what are the causes of wernicke’s encephalopathy?
main cause is alcohol abuse
rarer causes: persistent vomiting, stomach cancer, dietary insufficiency
what are the symptoms of wernicke’s encephalopathy?
mental slowing, impaired concentration, and apathy confusion, altered GCS ataxia ophthalmoplegia nystagmus (the most common ocular sign)
what investigations should your order for wernicke’s encephalopathy?
therapeutic trial of parenteral thiamine finger prick glucose FBC serum electrolytes renal function LFT urinary and serum drug screen serum ammonia blood alcohol level blood thiamine and metabolites
how is wernicke’s encephalopathy treated?
stabilisation and IV thiamine and IV magnesium sulfate and multivitamins
if there is ongoing risk of wernicke’s encephalopathy - give dietary supplementation with thiamine
what is korsakoff’s syndrome?
anterograde amnestic syndrome with disproportionate impairment of recent memory relative to other cognitive domains, accompanied sometimes with confabulation as a long term consequence of thiamine deficiency
degeneration of the mammillary bodies
often no complete recovery of memory deficit
what is Huntington’s disease?
an autosomal dominant neurogenerative disorder.
it is a progressive and incurable condition that typically results in death 20 years after the initial symptoms develop
it is a trinucleotide repeat disorder repeat expansion of CAG which results in degeneration of cholinergic and GABAergic neurones in the striatum of the basal ganglia
what are the typical features of huntington’s disease?
chorea (jerky involuntary movement)
personality changes (irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movement
loss of coordination
deficit in fine motor coordination (finger tapping)
impaired tandem walking
what investigations would you perform for huntington’s?
diagnosis is clinical
consider CAG repeat testing
PCR
Capillary or gel electrophoresis
MRI or CT scan
how is huntington’s managed?
counselling for patients and family
if there is chorea - antipsychotics or benzodiazepines
if there is depression - antidepressants - citalopram or fluoxetine
behaviour problems and mood instability - carbamazepine or valproic acid
behavioural problems where anxiety or insomnia is prominent (SSRI or benzodiazepines)
anxiety without prominent behavioural problems - SSRI
OCD behaviours - SSRI or antipsychotics or clomipramine or CBT
If there is bradykinesia and rigidity predominant - dopamine agonists (levodopa)
what is parkinson’s disease?
chronic progressive neurological disorder characterised by motor symptoms of resting tremor, rigidity, bradykinesia and postural instability.
what is the pathophysiology of parkinson’s?
there is loss of dopaminergic neurones in the substantia nigra with findings of lewy bodies in the affected neurones.
loss of these neurones within the basal ganglia accounts of the constellation of motor symptoms.
what are the clinical features of parkinson’s?
bradykinesia (slow movements) resting tremor - typically pill rolling rigidity - cogwheel - due to superimposed tremor postural instability - develops later shuffling gait stooped posture drooling psychiatric features impaired olfaction (smelling)
