neurological Flashcards
who gets strokes/TIAs
people >65
two main types of stroke
ischaemic stroke
haemorrhagic stroke
what causes ischaemic stroke
blood vessel blocked by something - fatty material/clot
thrombotic - blood clot spontaneously forms in artery in brain, complication of atherosclerosis
embolic - part of athersclerotic plauqe or clot breaks off and travels until trapped by narrow artery in brain - e.g. in AF
causes of haemorrhagic stroke
intracerebral haemorrhagic stroke - bleeding from blood vessel within brain. high blood pressure is biggest cause
subarachnoid haemorrhage - bleeding between brain and arachnoid matter
risk factors for TIA/stroke
thromboembolic stroke - hypertension, diabetes, smoking, hyperlipidaemia
also obesity, COCP, excessive alcohol consumption, polycythemia
AF - big risk factor
migraine, vascultitis and cocaine cause stroke by vasoconstriction
presentation of TIA/stroke
carotid territory symptoms - amaurosis fugax: transient loss of vision, aphasia, hemiparesis, hemisensory loss, hemianopic loss
vertebrobasilar territory symptoms: diplopia, vertigo, vomiting, choking, dysarthria, ataxia, hemisensory loss, menianopic or bilateral vision loss, tetraperesis, loss of consciousness
investigations for TIA/stroke
blood - glucose, FBC, ESR, creatinine, electrolytes, cholesterol, INR
brain imaging - MRI, CT
carotid artery imaging - doppler to look for atheroma and stenosis, MR angiography or CT angiography if US suggests carotid stenosis to determine degree of stenosis
treatment of ischaemic stroke
aspirin 300mg initially
continued long term 75g aspirin with 200mg TDS modified dipyridamole
clopidogrel instead of aspirin if needed
lifestyle changes for secondary prevention
carotid endarterectomy in patients with carotid artery stenosis
treatment of haemorrhagic stroke
anticoagulants should be stopped and their effects reversed by prothrombin complex concentrates
neurosurgical refferal to those with large intracerebral haematoma (deepening coma or brainstem compression etc)
who gets subarachnoid haemorrhage
mean age 50 yo
5% of strokes
causes of subarachnoid haemorrhage
spontaneous arterial bleeding into subarachnoid space caused by:
- saccular berry aneurysms (70%)- acquired lesions at branching points of major arteries coursing through subarachnoid space at circle of willis
congenital arteriovenous malformations - 10%
unknown cause
risk factors for subarachnoid haemorrhage
high blood pressure risk factors
presentation of subarachnoid haemorrhage
sudden onset severe headache
often occipital
maximum intensity within minutes (worst ever)
accompanied by nausea and vomiting and sometimes LOC
signs on examination of subarachnoid haemorrhage
signs of meningeal irritation - neck stiffness and positive kernings sign
focal neurological signs and subhyaloid haemorrhages (between retina and virteous membrane) with or without papilloedema.
some patients experience a warning headahce a few days before
investigation of subarachnoid haemorrhage
immediate CT - shows subarachnoid or intravascular blood in 24 hrs
lumbar puncture indicated if strong clinical suspician of SAH but CT is normal
increase in pigments (bilirubin and/or oxyhaemaglobin released from lysis and phagocytosis of RBC) = key finding. 12hrs after onset to 2 weeks
MR angiography to establish source for potential surgical patients
treatment of subarachnoid haemorrhage
cautious control of hypertension, bed rest and supportive management
nimodipine (calcium channel blocker) to reduce cerebral artery spasm
obliteration of aneurysms by surgical clipping or insertion of fine wire coil under radiological guidance prevents re-bleeding
lifestyle changes
causes of peripheral neuropathy
result of damage to nerves located outside brain and spinal cord. 6 core principles causing nerves to malfunction:
- demyelination
- axonal degeneration (toxin)
- wallerian degeneration following nerve section
- compression
- infarction (arteritis)
- infiltration by inflammatory cells (sarcoid)
health conditions that can cause: autoimmune diseases, diabetes, infections, inherited disorders, tumours, bone marrow disorder, also alcoholism, poisons, medications, truama/injury, vitamin deficiency
risk factors for peripheral neuropathy
DAMIT BITCH
Drugs and chemicals
Alcohol
Metabolic - diabetes, hypoglycaemia, uraemia
Infection
Tumour (paraneoplastic phenomenon)
B12 and other vitamin deficiencies
Idiopathic and infiltrative (amyloidosis)
Toxins
Connective tissue diseases and congenital
Hypothyroidism
presentation of peripheral neuropathy
sensory - gradual onset of numbness, prickling or tingling spreading upwards into legs and arms. extreme sensitivity to touch,
motor - lack of coordination and muscle weakness
autonomic nevres - heat intolerance, excessive sweating or nil sweat, bowel, bladder or digestive problems, postural hypotension, erectile dysfunction, arrythmias
investigations of peripheral neuropathy
blood tests - vitamin deficiences, diabetes, immune function
imaging - CT or MRI for herniated discs, pinched nerves etc
nerve function tests - EMG, thin needle electrodes, nerve conduction study
nerve or skin biopsy
treatment of peripheral neuropathy
manage underlying conditions
healthy lifestyle choices
medications - pain releivers, antiseizure meds (gabapentin+ pregabalin), topical treatments (capsaicin, lidocaine patches) and antidepressants
therapies - TENS, palsam exchange and IV immuen globulin, physical therapy, surgery
who gets epilepsy/seizures
bimodal incidence - children or >60yo
learning disabilities
often falsely diagnosed
causes of epilepsy/seizures
alcohol stroke intracranial haemorrhage space occupying lesion metabolic disturbance
risk factors of epilepsy/seizures
FH genetic conditions previous febrile seizures previous intracranial infections brain trauma surgery comorbid conditions - CVD or cerebral tumours
tonic seizure presentation
impairment of consciousness and stiffening (trunk straight or flexed at waist)
clonic seizure presentation
jerking and impairment of consciousness
typical absense seizures
begin in childhood
sharp onset and no residual symptoms
normal activity interrupted and child stares for few seconds
eyelids may twitch and some v small jerking movements of the hands may occur
lasts 5-10 seconds and less than 30 sec
can occur hundreds of times a day in children
myoclonic seizures
brief shock like contraction of limbs without the apparent impairment in consciousness
atonic seizures
sudden brief attacks of loss of tone associated with falls and retained consicousness
features of focal seizures
Temporal lobe - Automatisms (eg. lip-smacking); déjà vu or jamais vu, emotional disturbance (eg. sudden terror); olfactory, gustatory, or auditory hallucinations.
Frontal lobe - Motor features such as Jacksonian features, dysphasia, or Todd’s palsy.
Parietal lobe - Sensory symptoms such as tingling and numbness; motor symptoms - due to spread of electrical activity to the pre-central gyrus in the frontal lobe.
Occipital lobe - Visual symptoms such as spots and lines in the visual field.
investigaition of seizures
cardiac, neurological mental state and development assessment if possible
baseline tests for adults - FBC, U+Es, LFTs, glucose and calcium
12 lead ECG
treatment of seizures
prolonged seizure or repeated seizure (>3min) = rectal or IV diazepam or lorazepam
status epilepticus = rectal diazepam or buccal midazolam
prevent attacks drugs are specific to type of seizure: tonic clonic = sodium volproate, lamotrigine, carbamazepine, topiramate, penytoin
causes of meningitis
inflammation of the meninges as a reuslt of bacterial infection
- neisseria meningitides = meningococcal disease
- streptococcus pneumoniae = pneumococcal disease
- haemophilus influenza type B (most common children <3months)
risk factors of meningitis
young age winter season absent or non functioning spleen >65 immunocompromised organ dysfunction smoking crowded housing basal skull fractures with leakage of CSF cochlear implants otitis media sinusitis sickle cell disease
presentation of meningitis
non blanching rash fever vomiting/nausea lethargy irritability/unsettled behaviour ill appearance refusing food/drink headache msucle ache/joint pain respiratory symptoms/signs or breathing difficulty
signs on examination of meningitis
non blanching rash stiff neck cap refill >6 sec +cold hands and feet unusual skin colour shock and hypotension leg pain back ridigity bulging fontanelle photophobia kernings sign (unable to fully extend at knee when hip flexed) brudzinskis sign (persons knee and hip flex when neck flexed) unconscious or toxic moribund state paresis seizures
investigations for meningitis
head CT if suspicion of intracranial mass lesion such as focal neurological signs, papilloedema, LOC, seizures
lumbar puncture
- urgent CSF microscopy
- white cell count and differential and analysis for protein and glucose concentration
blood cultures, glucose, CXR, viral and syphillis serology
treatment of meningitis
admit to hospital as emergency 999
administer parenteral benzyl penicillin at earliest opportunity
cefotaxime 2g 6 hourly IV for initial treatment
add ampicillin 2g 4 hourly if immunosuppressed
follow sensitivity results
who gets migraines?
18% prevalence
mean age of onset = 18yo
causes of migraines
unknown
genetic and environmental factors
changes in brainstem and interactions with trigeminal nerve may be involved
risk factors of migraines
genetic - first degree relative
sex
age - peak at 30yo
hormonal changes
3 types of migraine
with aura
without aura
migraine variants (unilateral motor or sensory symptoms resembling a stroke)
typical migraine headache
unilateral
throbbing
build up over minutes to hours
presentation of migraine
heaches nausea vomiting photophobia irritable and prefers dark fatigue, nausea etc may occur hours to days before auras aphasia, tingling, numbness, weakness on one side of body
treatment of migraine
mild attacks = simple analgesia + antimetic such as metoclopramide
moderate/severe attacks = triptans are serotonin agonists (inhibit release of vasoconstirctive peptides)
- contraindicated in vascular disease
prophylactically (if >2 attacks per month) = pizotifen, beta blockers
causes of parkinsons disease
progressive depletion of dopamine secreting cells in substantia nigra
other causes of parkinsonism: drug induced, CVD, lewy body dementia, multiple system atrophy, progressive supranuclear palsy
parkinsonism
bradykinesa+
ridgity, tremor, postural instability
risk factors for parkinsons
clustering of early onset PD in some families
linked to mutations in a synuclein
presentation of parkinsons
unilaterally initially but becomes bilateral as disease progresses
slow progression
bradykinesia, hypokinesia, sitffness and ridigity, resting tremor, postural instability,
depression, anxiety, fatigue, reduced sense of smell, cognitive impairment, sleep disturbance, constipation
treatment of parkinson’s disease
levodopa + peipheral decarboxylase inhibitor (carbidopa or beserazide) = control peripheral side effects
dopamine agonists
monoamine oxidase B inhibitor = inhibit catabolism of dopamine in brain
what is proximal myopathy
symmetrical weakness of te proximal upper and/or lower limbs
causes of proximal myopathy
drugs alcohol thyroid disease osteomalacia idiopathic inflammatory myopathies hereditary myopathies malignancy infections sarcoidosis
aim of clinical assessment of proximal myopathy
distinguish proximal myopathy from other conditions that can present similarly
identify patients who need prompt attention - cardiac, resp or pharyngeal muscle involvement
determine underlying cause
investigations for proximal myopathy
creatine kinase, thyroid function and OH vitamin D levels
further evaluation - neurological studies, muscle imaging and muscle biopsy in those whom no toxic, metabolic or endocrine cause is found and those with clinical features suggestive of inflammatory or hereditary myopathy
treatment of proximal myopathy
depends on underlying cause
remove offending agent, correction of endocrine or metabolic problem, corticosteroids and immunosuppressive therapy for IIM and physical therapy and genetic counselling for muscular dystrophies
who gets multiple sclerosis
begins in early adulthood
more common in women
what causes multiple sclerosis
multiple plaques of demyelination within the brain and spinal cord
inflammatory process
thought that exposure to infectious agent in childhood EBV may predispose
what is MS
inflammation, demyelination and axonal loss
presentation of MS
young adult with 2 or more clinically distinct episodes of CNS dysfunction followed by remission
relapsing/remitting MS = optic neuropathy, brainstem demyelination and spinal cord lesions
investigations of MS
MRI of brain and spinal cord is definitive test
treatment of MS
short courses of steroids
subcut beta-interferon reduces relapse rate by 1/3 in relapsing/remitting disease
physio + other drug options to consider
3 catagories of focal seizures
complex = impairment of consciousness
simple = no LOC
secondary generalised = focal evolves to generalised
4 types of general seizure
absence
tonic-clonic
myoclonic
atonic
treatment of absence seizure
valproate or ethosuximide
what not to give in absence seizure
carbamazepine
treatment of tonic clonic seizure
volproate or lamotrigine
treatment of myoclonic seizure
valproate
or levitiraetam or topiramide if preg
what not to give myoclonic seizures
carbamazepine
atonic seizure treatment
valproate or lamotrigine
treatment of focal seizures
carbamazepine or lamotrigine
complications of seizures
status epilepticus
depression
suicide
SUDEP (due to cardiac arrhithmia)
treatment of status epilepticus
iv lorazepam
buccal midazolam
if not work - phenytoin and call anaesthetist
