neurological Flashcards

(72 cards)

1
Q

who gets strokes/TIAs

A

people >65

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2
Q

two main types of stroke

A

ischaemic stroke

haemorrhagic stroke

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3
Q

what causes ischaemic stroke

A

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

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4
Q

causes of haemorrhagic stroke

A

intracerebral haemorrhagic stroke - bleeding from blood vessel within brain. high blood pressure is biggest cause

subarachnoid haemorrhage - bleeding between brain and arachnoid matter

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5
Q

risk factors for TIA/stroke

A

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

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6
Q

presentation of TIA/stroke

A

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

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7
Q

investigations for TIA/stroke

A

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

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8
Q

treatment of ischaemic stroke

A

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

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9
Q

treatment of haemorrhagic stroke

A

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)

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10
Q

who gets subarachnoid haemorrhage

A

mean age 50 yo

5% of strokes

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11
Q

causes of subarachnoid haemorrhage

A

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

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12
Q

risk factors for subarachnoid haemorrhage

A

high blood pressure risk factors

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13
Q

presentation of subarachnoid haemorrhage

A

sudden onset severe headache
often occipital
maximum intensity within minutes (worst ever)
accompanied by nausea and vomiting and sometimes LOC

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14
Q

signs on examination of subarachnoid haemorrhage

A

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

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15
Q

investigation of subarachnoid haemorrhage

A

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

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16
Q

treatment of subarachnoid haemorrhage

A

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

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17
Q

causes of peripheral neuropathy

A

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

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18
Q

risk factors for peripheral neuropathy

A

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

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19
Q

presentation of peripheral neuropathy

A

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

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20
Q

investigations of peripheral neuropathy

A

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

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21
Q

treatment of peripheral neuropathy

A

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

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22
Q

who gets epilepsy/seizures

A

bimodal incidence - children or >60yo
learning disabilities
often falsely diagnosed

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23
Q

causes of epilepsy/seizures

A
alcohol
stroke
intracranial haemorrhage
space occupying lesion
metabolic disturbance
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24
Q

risk factors of epilepsy/seizures

A
FH
genetic conditions
previous febrile seizures
previous intracranial infections
brain trauma
surgery
comorbid conditions - CVD or cerebral tumours
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25
tonic seizure presentation
impairment of consciousness and stiffening (trunk straight or flexed at waist)
26
clonic seizure presentation
jerking and impairment of consciousness
27
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
28
myoclonic seizures
brief shock like contraction of limbs without the apparent impairment in consciousness
29
atonic seizures
sudden brief attacks of loss of tone associated with falls and retained consicousness
30
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.
31
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
32
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
33
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)
34
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 ```
35
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 ```
36
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 ```
37
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
38
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
39
who gets migraines?
18% prevalence | mean age of onset = 18yo
40
causes of migraines
unknown genetic and environmental factors changes in brainstem and interactions with trigeminal nerve may be involved
41
risk factors of migraines
genetic - first degree relative sex age - peak at 30yo hormonal changes
42
3 types of migraine
with aura without aura migraine variants (unilateral motor or sensory symptoms resembling a stroke)
43
typical migraine headache
unilateral throbbing build up over minutes to hours
44
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 ```
45
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
46
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
47
parkinsonism
bradykinesa+ ridgity, tremor, postural instability
48
risk factors for parkinsons
clustering of early onset PD in some families linked to mutations in a synuclein
49
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
50
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
51
what is proximal myopathy
symmetrical weakness of te proximal upper and/or lower limbs
52
causes of proximal myopathy
``` drugs alcohol thyroid disease osteomalacia idiopathic inflammatory myopathies hereditary myopathies malignancy infections sarcoidosis ```
53
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
54
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
55
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
56
who gets multiple sclerosis
begins in early adulthood more common in women
57
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
58
what is MS
inflammation, demyelination and axonal loss
59
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
60
investigations of MS
MRI of brain and spinal cord is definitive test
61
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
62
3 catagories of focal seizures
complex = impairment of consciousness simple = no LOC secondary generalised = focal evolves to generalised
63
4 types of general seizure
absence tonic-clonic myoclonic atonic
64
treatment of absence seizure
valproate or ethosuximide
65
what not to give in absence seizure
carbamazepine
66
treatment of tonic clonic seizure
volproate or lamotrigine
67
treatment of myoclonic seizure
valproate | or levitiraetam or topiramide if preg
68
what not to give myoclonic seizures
carbamazepine
69
atonic seizure treatment
valproate or lamotrigine
70
treatment of focal seizures
carbamazepine or lamotrigine
71
complications of seizures
status epilepticus depression suicide SUDEP (due to cardiac arrhithmia)
72
treatment of status epilepticus
iv lorazepam buccal midazolam if not work - phenytoin and call anaesthetist