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Osha 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

Describe symptoms of an extradural bleed

A
  • developed a headache after head trauma
  • confused and drowsy
  • difficult to rouse
  • biconvex shape on CT
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2
Q

What is an extradural haemorrhage?

A
  • usually caused by rupture of middle meningeal artery
  • in temporo-parietal region
  • associated with fracture of temporal bone
  • occurs between skull and dura mater
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3
Q

Where does a subdural haemorrhage occur?

A
  • rupture of bridging veins in outermost meningeal layer
  • occurs between dura mater and arachnoid mater
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4
Q

Describe the presentation of subdural bleeding

A
  • crescent shape on CT and possible midline shift
  • drowsiness, reduced consciousness, high ICP
  • seizure
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5
Q

What is the pathophysiology behind subdural bleeding?

A
  • usually occurs due to trauma
  • turning/jerking injuries cause damage to the bridging veins and causes tears
  • elderly and alcoholics have more brain atrophy making rupture more likely
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6
Q

Describe presentation of subarachnoid bleeding

A
  • sudden onset
  • severe thunderclap headache
  • occurs due to strenuous activity
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7
Q

What is Guillan-Barré syndrome?

A
  • an acute paralytic polyneropathy
  • affects peripheral nervous system
  • symptoms peak after 2-4 weeks, recovery can take months-years
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8
Q

What causes Guillan-Barré syndrome?

A
  • triggered by infection
  • associated with:
  • campylobacter jejuni (MC)
  • cytomegalovirus
  • Epstein-Barr virus
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9
Q

What is the pathophysiology behind Guillan-Barré syndrome?

A
  • occurs due to molecular mimicry
  • B cells create antibodies against antigens on the pathogen
  • these antibodies match proteins on nerve cells
  • Abs then target myelin sheath of motor nerve cell or nerve axon
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10
Q

How does Guillan-Barré syndrome present?

A
  • symmetrical ascending weakness (starting at feet)
  • reduced reflexes
  • peripheral loss of sensation/neuropathic pain
  • progresses to cranial nerves and causes facial weakness
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11
Q

How is Guillan-Barré syndrome diagnosed?

A
  • Brighton criteria
  • nerve conduction studies
  • lumbar puncture for CSF: raised protein, normal cell count and glucose
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12
Q

How is Guillan-Barré syndrome managed?

A
  • IV immunoglobulins
  • plasma exchange
  • supportive care
  • VTE prophylaxis
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13
Q

What is multiple sclerosis?

A
  • chronic and progressive condition involving demyelination of neurones in the CNS
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14
Q

What is the epidemiology of multiple sclerosis?

A
  • young adults (under 50)
  • more common in women
  • symptoms improve in pregnancy and postpartum
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15
Q

What is the pathophysiology of multiple sclerosis?

A
  • myelin provided by Schwann cells in PNS and oligodendrocytes in CNS
  • inflammation around myelin and infiltration of immune cells damages myelin causing symptoms
  • re-myelination can occur in early disease, is incomplete in late disease > permanence
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16
Q

Why do symptoms of MS change over time?

A
  • lesions vary in location over time
  • different nerves are affected and symptoms change
  • lesions are disseminated in time and space
  • early course: relapsing-remitting attacks
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17
Q

What is the aetiology of multiple sclerosis?

A
  • genetic
  • EBV
  • low vit D
  • smoking
  • obesity
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18
Q

What optical symptoms occur with multiple sclerosis?

A
  • double vision: abducens (VI) lesions
  • internuclear opthalmoplegia: problems with coordinating eye movements (III, IV, VI)
  • conjugate lateral gaze disorder: affected eye cannot abduct (VI)
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19
Q

What is optic neuritis?

A
  • unilateral reduced vision over hours to days
  • central scotoma (enlarged blind spot)
  • impaired colour vision
  • pain on eye movement
  • relative afferent pupillary defect
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20
Q

What is the general presentation of multiple sclerosis?

A
  • sensory and cerebellar ataxia
  • tremors
  • incontinence
  • limb paralysis
  • trigeminal neuralgia, numbness and paresthesia
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21
Q

How is multiple sclerosis diagnosed?

A
  • progressive symptoms over a year
  • or 2 attacks disseminated in time and space
  • MRI brain + cord showing lesions
  • LP shows oligoclonal IgG bands in CSF
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22
Q

What are the types of disease course of multiple sclerosis?

A
  • relapsing-remitting: episodes of disease followed by recovery - can be active and/or worsening
  • 1º progressive: gradual deterioration without recovery
  • 2º progressive: relapsing-remitting > worsening and incomplete remission
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23
Q

How is multiple sclerosis managed?

A
  • acute episodes: IV methylprednisolone
  • DMDs: β interferon
  • mitoxantrone
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24
Q

What are differential diagnoses for multiple sclerosis?

A
  • SLE, Sjrogen’s, encephalomyelitis
  • Lyme’s, syphilis, AIDS
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25
Q

What is Parkinson’s disease?

A
  • progressive reduction of dopamine in the basal ganglia leading to movement disorders
  • substantia nigra produces dopamine
  • asymmetrical symptom
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26
Q

What are the risk factors and epidemiology of Parkinson’s?

A
  • family history
  • male
  • inc age
  • e.g. 70y/o male
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27
Q

What are the symptoms of Parkinson’s?

A
  • unilateral tremor: 4-6Hz
  • cogwheel rigidity: jerky movement
  • bradykinesia: shuffling gait, difficulty initiating movement, reduced facial expression
  • anosmia
  • postural instability
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28
Q

How is Parkinson’s diagnosed and what is the classic triad?

A
  • clinically based on symptoms
  • resting tremor, rigidity, bradykinesia
  • DaTscan
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29
Q

How is Parkinson’s managed?

A
  • Levodopa + decarboxylase inhibitor
  • dopamine agonist e.g. bromocriptine
  • COMT inhibitors e.g. entacapone: metabolises L-dopa
  • Monoamine oxidase B inhibitors - rasagiline
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30
Q

How does levodopa work and what are the associated side effects?

A
  • synthetic dopamine e.g. carbidopa
  • taken alongside decarboxylase inhibitor e.g. benserazide
  • becomes less effective over time
  • leads to dyskinesias e.g. dystonia, chorea, athetosis
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31
Q

What is Huntington’s chorea and what is the pathophysiology?

A
  • autosomal dominant condition with full penetrance
  • trinucleotide repeat disorder in HTT in chromosome 4
  • lack of GABA and excessive nigrostriatal pathway
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32
Q

What is genetic anticipation?

A
  • more trinucleotide repeats leads to earlier onset of disease and increased severity
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33
Q

When does Huntington’s present and what is the prognosis?

A
  • asymptomatic until age 30-50
  • life expectancy: 15-20yrs after onset of symptoms
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34
Q

How does Huntington’s present?

A
  • cognitive, psychiatric and mood problems > movement disorder
  • chorea
  • eye movement disorders
  • dysarthria and dysphagia
  • depression
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35
Q

How is Huntington’s diagnosed?

A
  • genetic testing with pre and post-test counselling
  • diagnosis if > 35 CAG repeats
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36
Q

How is Huntington’s managed?

A
  • antipsychotics e.g. olanzapine
  • benzodiazepines e.g. diazepam
  • dopamine-depleting agents e.g. tetrabenzine
  • antidepressants
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37
Q

What is myasthenia gravis?

A
  • autoimmune condition causing muscle weakness
  • progressively worse weakness with activity which improves with rest
  • mostly affects proximal muscles and small muscles of head and neck
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38
Q

What is the epidemiology of myasthenia gravis?

A
  • women under 40
  • men over 60 (more related to thymoma)
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39
Q

What is the pathophysiology behind myasthenia gravis?

A
  • Ach-R antibodies bind to postsynaptic NMJ receptors
  • Ach unable to bind, stimulate receptor and trigger muscle contraction
  • more used during activity and so more are blocked
  • Abs activate complement system leading to damage at postsynaptic membrane
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40
Q

How does myasthenia gravis present?

A
  • extraocular muscle weakness > diplopia
  • eyelid weakness > ptosis
  • dysphagia
  • jaw fatigue
  • slurred speech
  • facial weakness
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41
Q

How can myasthenia gravis be examined?

A
  • repeated blinking > ptosis
  • prolonged upward gazing > diplopia
  • repeated abduction of one arm > unilateral weakness
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42
Q

How is myasthenia gravis diagnosed?

A
  • testing for antibodies: acetylcholine receptor (Ach-R) and muscle-specific kinase (MuSK)
  • Edrophonium test
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43
Q

What is the edrophonium test for myasthenia gravis?

A
  • IV dose of edrophonium chloride
  • normally cholinesterase enzymes break down Ach but edrophonium blocks the enzymes
  • stops Ach breakdown and and inc Ach levels
  • relieves weakness temporarily
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44
Q

How is myasthenia gravis managed?

A
  • reversible Ach inhibitors: pyridostigmine
  • immunosuppression
  • thymectomy
  • monoclonal Abs: rituximab
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45
Q

What is myasthenic crisis?

A
  • complication causing acute worsening of symptoms
  • triggered by another illness e.g. resp tract
  • can lead to resp failure > ventilation
  • treatment with IVIG and plasma exchange
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46
Q

What is the pathophysiology of trigeminal neuralgia?

A
  • can affect any combination of V1, V2 and V3
  • 90% cases are unilateral
  • triggers: cold weather, spicy food, caffeine, citrus
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47
Q

What are the 3 branches of the trigeminal nerve?

A
  • V1: ophthalmic
  • V2: maxillary
  • V3: mandibular
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48
Q

What is the presentation of trigeminal neuralgia?

A
  • intense facial pain
  • comes on spontaneously, can last seconds to hours
  • electricity-like shooting pain
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49
Q

How is trigeminal neuralgia treated?

A
  • carbamazepine
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50
Q

How do tension headaches present?

A
  • mild ache across forehead in band like pattern
  • muscle ache in frontal, temporalis and occipitalis muscles
  • come on and resolve gradually: no visual changes
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51
Q

What are the causes of tension headaches?

A
  • alcohol
  • depression
  • dehydration
  • stress
  • skipping meals
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52
Q

What are cluster headaches?

A
  • severe and unbearable unilateral headaches
  • usually around the eye
  • crescendo pain which may affect temples
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53
Q

Who is the typical patient to suffer from cluster headaches?

A
  • 30-50 y/o male smoker
  • attacks triggered by: alcohol, strong smells, exercise
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54
Q

What is the frequency of cluster headaches?

A
  • attacks lasting 15 mins - 3hrs
  • may suffer multiple attacks per day for weeks or months
  • followed by pain free period lasting 1-2 years
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55
Q

What are the symptoms of cluster headaches?

A
  • unilateral
  • red, swollen, watering eye
  • pupil constriction
  • ptosis
  • nasal discharge
  • facial sweating
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56
Q

What are the types of migraines?

A
  • migraine with or without aura
  • silent migraine (with aura but without headache
  • hemiplegic migraine
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57
Q

What are migraine triggers?

A
  • stress
  • bright lights
  • strong smells
  • dehydration
  • menstruation
  • abnormal sleep patterns
  • certain foods e.g. chocolate, cheese, caffeine
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58
Q

What are the symptoms of migraine?

A
  • pounding/throbbing
  • usually unilateral
  • photophobia and phonophobia
  • nausea and vomiting
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59
Q

What is aura?

A
  • visual changes
  • sparks in vision
  • blurring lines
  • lines across vision
  • loss of visual field
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60
Q

What is the treatment for migraine?

A
  • paracetamol
  • triptans e.g. sumatriptan
  • NSAIDs
  • antiemetics
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61
Q

How do triptans work?

A
  • 5HT receptor agonists (serotonin)
  • cause vasoconstriction in artery smooth muscle
  • inhibit peripheral pain receptors
  • reduce neuronal activity in CNS
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62
Q

What is prophylaxis for migraine?

A
  • headache diary
  • propanolol, topiramate, amitriptyline
  • acupuncture
  • riboflavin
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63
Q

What is epilepsy?

A
  • an umbrella term for a condition where there is a tendency to have seizures
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64
Q

What is a seizure?

A
  • a transient episode of electrical activity due to abnormally excessive or synchronous neuronal activity within the brain
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65
Q

What are the causes of seizures?

A
  • vascular
  • idiopathic
  • infection
  • trauma
  • dementia and drugs
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66
Q

What are some seizure triggers?

A
  • fatigue
  • stress
  • alcohol and drugs
  • flashing lights
  • monthly periods
  • missing meals
  • fever
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67
Q

What is the pathophysiology behind epileptic seizures?

A
  • normal balance between GABA and glutamate
  • balance shifts towards glutamate
  • more excitatory > inc glutamate stimulation and inc GABA inhibition
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68
Q

How is epilepsy diagnosed?

A
  • electroencephalogram: electrical activity in brain
  • MRI brain
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69
Q

What is a generalised tonic-clonic seizure?

A
  • loss of consciousness with muscle tensing (tonic) and muscle jerking (clonic) movements
  • tonic phase occurs before clonic
  • post-ictal period
  • limb contraction, extension, back arching and - usually last 2-3 minutes
  • ictal cry: sound resulting from chest contraction
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70
Q

What symptoms are experienced in the postictal period?

A
  • amnesia
  • postictal nose wiping (ipsilateral)
  • confusion, irritability, feeling low
  • sore tongue from bitten
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71
Q

What is an absence seizure?

A
  • commonly in school aged children
  • becomes blank and stares into space then abruptly returns to normal
  • unaware of their surroundings and unresponsive but still conscious
  • Episodes last 10-20 seconds and can disappear with age
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72
Q

What is the difference between tonic and atonic seizures?

A
  • Tonic: person becomes stiff suddenly
  • Atonic: known as drop attacks where all muscles relax at once (lapse in muscle tone). These don’t tend to last for more than 3 minutes
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73
Q

What is a myoclonic seizure?

A
  • sudden, brief muscle contractions like a jump
  • Seizures are brief but can occur in clusters, usually shortly after waking up
  • Patient remains conscious.
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74
Q

What is a complex partial seizure?

A
  • consciousness may be impaired
  • Often occurs in the temporal lobe
  • May have post-ictal confusion
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75
Q

What is a focal seizure?

A
  • only one part of the brain is affected
  • Can be aware or unaware
  • start in the temporal lobes and can affect hearing, speech, memory and emotions.
  • Presentation: hallucination, flashbacks, deja vu, doing things on autopilot.
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76
Q

What are the symptoms of focal aware (partial) temporal and frontal lobe seizures?

A
  • Temporal: rising feeling in stomach, deja vu, unusual taste or smells, intense feelings of fear or joy
  • Frontal: ‘wave feeling’ going through head, stiffness or twitching in a limb
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77
Q

What are the symptoms of focal aware (partial) parietal and occipital lobe seizures?

A
  • Parietal: numbness or tingling, arms or legs feel bigger or smaller than normal
  • Occipital: visual disturbance (coloured or flashing lights), hallucinations
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78
Q

How is epilepsy investigated?

A
  • electroencephalogram (EEG) shows typical patterns
  • MRI brain
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79
Q

What is the treatment for epilepsy?

A
  • sodium valproate
  • lamotrigine for child bearing aged women
  • carbamazepine: 1st line for focal seizure
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80
Q

How does sodium valproate work and what are the side effects?

A
  • increases activity of GABA: has relaxing effect
  • inhibits sodium ion channels
  • teratogenic, liver damage, hair loss, tremor
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81
Q

What is an ischaemic stroke?

A
  • 85% cases
  • a long TIA
  • caused by thrombosis/AF embolisation
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82
Q

What is a haemorrhagic stroke?

A
  • 15% cases
  • ruptured blood vessel
  • caused by trauma, htn, berry aneurysm rupture
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83
Q

What are general symptoms of an anterior circulation stroke?

A
  • hemiparesis
  • hemisensory loss
  • visual field defect (homonymous hemianopia withOUT macular sparing)
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84
Q

What are symptoms of an anterior circulation dominant hemisphere stroke?

A
  • usually in left hemisphere
  • expressive and receptive dysphagia
  • dyslexia
  • dysgraphia
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85
Q

What are symptoms of an anterior circulation non-dominant hemisphere stroke?

A
  • anosognosia
  • visuospatial dysfunction: geographical agnosia, dressing and constructional apraxia
86
Q

What are symptoms of a posterior circulation stroke?

A
  • often affects cerebellum + occipital lobe
  • clumsiness, difficulty walking in straight line
  • visual disturbance
  • slurred speech
  • headache, vomiting
87
Q

What investigations are done for stroke?

A
  • 1st line: CT head
  • gold: diffusion weighted MRI
  • blood test
  • carotid doppler
88
Q

What is the management for stroke?

A
  • aspirin 300mg stat and continued for 2 weeks
  • thrombolysis with alteplase (TPA) in 4.5 hr window
  • keep BP high to avoid reduced perfusion
89
Q

What are the secondary prevention guidelines for stroke?

A
  • Clopidogrel 75mg once daily
  • Atorvastatin 80mg started (not immediately)
  • Carotid endarterectomy or stenting
  • Treat modifiable risk factors
90
Q

What is subarachnoid haemorrhage?

A
  • bleeding into subarachnoid space between Pia mater and arachnoid membrane (where CSF is)
  • usually due to ruptured cerebral aneurysm
91
Q

What are the symptoms of a subarachnoid haemorrhage?

A
  • thunderclap headache described like being hit on the back of the head
  • neck stiffness
  • photophobia
  • visual changes
  • neurological symptoms
92
Q

What are the causes of subarachnoid haemorrhage?

A
  • cocaine use
  • sickle cell anaemia
  • connective tissue disorders
  • neurofibromatosis
  • autosomal dominant PKD
93
Q

What is the presentation of brain tumours?

A
  • varied dependent on tumour grade, site, type
  • headache
  • seizures
  • focal neurological symptoms
  • other non-focal symptoms e.g. cognitive problems or behavioural changes
94
Q

What is the epidemiology of subarachnoid haemorrhage?

A
  • black patients
  • female
  • age 45-70
95
Q

What are risk factors for subarachnoid haemorrhage?

A
  • htn
  • smoking
  • excess alcohol consumption
  • cocaine use
  • family history
96
Q

How is a subarachnoid haemorrhage investigated?

A
  • 1st line: NC CT head: hyperattenuation of blood in subarachnoid space
  • If negative: LP for CSF. Raised red cell count and xanthochromia (bilirubin)
  • If +ve: angiography
97
Q

What is the management of subarachnoid haemorrhage?

A
  • surgical intervention for aneurysms: endovascular coiling with catheter or clipping off
  • nimodipine: CCB that prevents vasospasm
98
Q

What are the symptoms of a raised ICP headache?

A
  • woken by headache
  • worse in the morning, lying down
  • exacerbated by coughing, sneezing, drowsiness
  • nausea and vomiting
99
Q

What are symptoms of a brain tumour?

A
  • raised ICP
  • Cushing’s triad
  • focal neurology
  • epileptic seizures
  • lethargy + weight loss
100
Q

What is Cushing’s triad?

A
  • bradycardia
  • irregular respiration
  • widened pulse pressure
101
Q

What is the investigation for suspected brain tumour?

A
  • MRI
  • biopsy
  • NO LP > contraindicated if high ICP
102
Q

What are some types of primary brain tumour?

A
  • astrocytoma
  • oligodendrocytoma
  • meningioma
  • Schwannoma
103
Q

Which cancers commonly metastasise to the brain?

A
  • lung
  • breast
  • renal cell carcinoma
  • melanoma
104
Q

What are the types of gliomas?

A
  • astrocytomas
  • oligodendroglioma
  • ependymoma
  • grade 1 are benign
  • grade 4 are most malignant: glioblastoma
105
Q

What is the treatment for brain tumours?

A
  • surgery: early resection
  • combined radiotherapy and chemotherapy
106
Q

What is an acoustic neuroma?

A
  • tumours of Schwann cells on auditory nerve
  • occur along cerebellopontine angle
  • symptoms: hearing loss, tinnitus, balance problems
107
Q

What is papilloedema?

A
  • swelling of optic disc 2º to raised ICP
  • blurring of optic disc margin
  • Elevated optic disc
  • Engorged retinal veins
  • Creases in the retina and haemorrhages around optic disc
108
Q

What are red flag features of headaches?

A
  • Constant
  • Nocturnal
  • Worse on waking
  • Worse on coughing, straining or bending forward
  • Vomiting
109
Q

What is motor neurone disease?

A
  • progressive, ultimately fatal condition
  • motor neurones stop functioning
110
Q

What are the types of motor neurone disease?

A
  • amyotrophic lateral sclerosis (ALS)
  • progressive bulbar palsy
  • progressive muscular atrophy
  • primary lateral sclerosis
111
Q

What is the pathophysiology behind motor neurone disease?

A
  • progressive degeneration of upper and lower motor neurones
  • sensory neurones spared
112
Q

What are risk factors for motor neurone disease?

A
  • genetic
  • smoking
  • SOD-1 mutation
  • exposure to heavy metals and pesticides
113
Q

What is the presentation of motor neurone disease?

A
  • progressive weakness of muscles affecting limbs, trunk, face, speech
  • weakness first noticed in upper limbs: fatigue when exercising
  • dysarthria
  • mixed LMN and UMN signs
114
Q

What are signs of lower motor neurone disease?

A
  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes
  • Babinski -ve
115
Q

What are the signs of upper motor neurone disease?

A
  • increased tone or spasticity
  • brisk reflexes
  • no fasciculation
  • babinski +ve: upgoing plantar responses
116
Q

What are the medications used for tremors?

A
  • primidone
  • β blockers
  • gabapentin
117
Q

What is the management of motor neurone disease?

A
  • riluzole: sodium channel blocker
  • edaravone
  • non-invasive ventilation to support breathing at night
118
Q

What is a transient ischaemic attack (TIA)?

A
  • transient neurological dysfunction secondary to ischaemia without infarction
  • often precede a stroke
  • caused by carotid thrombo-emboli
119
Q

What is the management of TIA?

A
  • 300mg aspirin as soon as suspected
  • followed by clopidogrel
120
Q

What is amaurosis fugax?

A
  • sudden loss of vision in one eye: veiling
  • caused by infarct in retinal arteries
  • retinal branches from ophthalmic which branches from int carotid
121
Q

What are the symptoms of a stroke in the anterior cerebral artery?

A
  • weak, numb, contralateral leg
122
Q

What are the symptoms of a stroke in the middle cerebral artery?

A
  • weak, numb, contralateral side of the body
  • facial drooping
  • forehead sparing
  • dysphasia (temporal lobe)
123
Q

What are the symptoms of a stroke in the posterior cerebral artery?

A
  • visual loss
  • contralateral homonymous hemaniopia with macular sparing
124
Q

What is the ABCD2 scoring system?

A
  • risk of stroke following TIA
  • Age >60 (1)
  • BP > 140/90 (1)
  • Clinical symptoms: unilateral weakness (2), slurred speech, no weakness (1)
  • duration Sx: >1h (2). <1hr (1)
  • T2DM (1)
125
Q

What are symptoms of meningitis?

A
  • fever
  • photophobia
  • neck stiffness
  • non-blanching petechial rash
  • vomiting
126
Q

What is Kernig’s test?

A
  • lie patient on back
  • flexing one hip and knee to 90 degrees and slowly straighten knee (keep the hip flexed)
  • spinal pain or resistance to movement in meningitis
127
Q

What is Brudisinski’s test?

A
  • lie patient on back
  • gently lift head and neck and flex chin to chest
  • patient will involuntarily flex hips and knees
128
Q

What is the management of meningitis?

A
  1. Assess GCS
  2. Blood cultures
  3. Broad spectrum antibiotics
  4. steroids e.g. dexamethasone
129
Q

What antibiotics are given for meningitis?

A
  • IV benzylpenicillin in primary care and immediate hospital referral
  • < 3mo: cefotaxime + amoxicillin
  • > 3mo: ceftriaxone
130
Q

What special considerations should be made when treating meningitis?

A
  • allergy to penicillin: if anaphylaxis switch to chloramphenicol
  • immunocompromised: potentially caused by listeria: add amoxicillin
  • recent travel: add vancomycin
131
Q

What are contraindications for a lumbar puncture?

A
  • abnormal clotting (platelets/coagulation)
  • petechial rash
  • raised ICP
132
Q

What are differential diagnoses for meningitis?

A
  • subarachnoid haemorrhage
  • migraine
  • flu and sinusitis
  • malaria
133
Q

What is the public health response to meningitis?

A
  • notify UK HSA
  • identify close contacts
  • PEP: ciprofloxacin or rifampicin for close contacts
134
Q

What is meningitis?

A
  • inflammation of the meninges (lining of the brain and spinal cord)
135
Q

What are the causes of meningitis?

A
  • infective: bacterial, viral, fungal, parasitic
  • non-infective: paraneoplastic, drugs, autoimmune
136
Q

How does bacteria causing meningitis enter the body?

A
  • extra cranial infection: nasal carriage, otitis media, sinusitis
  • via bloodstream: bacteraemic
  • neurosurgical complications: post op, infected shunts
137
Q

What is meningococcal septicaemia?

A
  • meningococcus bacterial infection in the bloodstream
  • causes the non blanching rash
  • infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages
138
Q

Which bacteria commonly cause meningitis?

A
  • Neisseria meningitidis (gram -ve diplococcus)
  • Strep pneumoniae (gram +ve cocci)
  • listeria monocytogenes (pregnancy)
  • group B strep in neonates
139
Q

What are the most common causes of viral meningitis?

A
  • HSV, enterovirus and VZV
  • CSF sample sent for PCR testing
  • treated with aciclovir
140
Q

What are the possible complications of meningitis?

A
  • hearing loss
  • cerebral palsy
  • seizures and epilepsy
  • cognitive impairment
  • disability
141
Q

What is the definition and presentation of encephalitis?

A
  • inflammation of the brain
  • flu-like illness
  • altered GCS, fever, seizures, memory loss
142
Q

What are the causes of encephalitis?

A
  • usually viral
  • herpes simplex
  • varicella zoster
143
Q

What are the investigations for encephalitis?

A
  • MRI head
  • LP: lymphocytic CSF and viral PCR
144
Q

What is the management of encephalitis?

A
  • supportive
  • aciclovir if HSV or VZV
145
Q

What is cauda equina syndrome?

A
  • nerve roots of cauda equina at bottom of spine are compressed
  • emergency
146
Q

What is the anatomy of the cauda equina?

A
  • collection of nerve roots travelling through spinal canal after cord terminates around L2/L3
  • spinal cord tapers down into conus medullaris
  • nerve roots exit at vertebral level
147
Q

What do the nerves of the cauda equina supply?

A
  • sensation to lower limbs, perineum, bladder, rectum
  • motor innervation to lower limbs, anal and urethral sphincters
  • parasympathetic innervation of bladder and rectum
148
Q

What is the aetiology of cauda equina syndrome?

A
  • herniated disc (most common)
  • (metastasised) tumours
  • spondylolisthesis
  • abscess and trauma
149
Q

What are signs of cauda equina syndrome?

A
  • saddle anaesthesia
  • loss of sensation in bladder and rectum
  • faecal incontinence
  • bilateral sciatica and motor weakness
150
Q

What is the management of cauda equina?

A
  • emergency MRI and neurosurgical input to consider lumbar decompression surgery
151
Q

What are the causes of spinal cord compression?

A
  • degenerative disc lesions
  • degenerative vertebral lesions
  • TB
  • vertebral neoplasms
  • epidural abscess or haemorrhage
152
Q

What is the presentation of spinal cord compression?

A
  • sensory loss below level of compression
  • spastic paraparesis/tetraparesis
  • radicular pain at level of compression
153
Q

Where is the sciatic nerve and what does it do?

A
  • L4-S3 form sciatic nerve
  • supplies sensation to lateral lower leg and foot
  • motor for posterior thigh, lower leg and foot
154
Q

What is sciatica?

A
  • unilateral pain from the buttock radiating down the back of the thigh to below the knee or foot
  • causes: herniated disc, spondylolisthesis, spinal stenosis
155
Q

What is the presentation of sciatica?

A
  • electric or shooting pain
  • paraesthesia
  • numbness
  • motor weakness
156
Q

What is dementia?

A
  • progressive global decline of cognitive function without impairment of consciousness
  • mild cognitive impairment (MCI) is seen as a pre-cursor
  • typically affects temporal and parietal lobes
157
Q

What is vascular dementia?

A
  • results from many small infarcts
  • step-wise progression
  • infarcts affect function if damaging white matter
158
Q

How can vascular dementia be prevented and which conditions is it associated with?

A
  • aspirin or warfarin therapy
  • controlling BP
  • raised BP, past strokes
159
Q

What is Lewy-body dementia?

A
  • presence of Lewy bodies in the brainstem and neocortex
  • fluctuating cognitive impairment
  • hallucinations and Parkinsonism
160
Q

What are the causes of peripheral neuropathy?

A
  • Diabetes
  • Alcoholism
  • Vitamin (B12) deficiency
  • Infective/inherited
  • Drugs
161
Q

What is the pathophysiology behind peripheral neuropathy (6 mechanisms)?

A
  1. demyelination (Schwann cell damage)
  2. axonal degeneration
  3. nerve fibres cut or crushed
  4. compression causing demyelination
  5. infarction
  6. infiltration by infection
162
Q

What are the aetiologies of secondary intracerebral haemorrhages?

A
  • clotting disorder
  • AV malformation
  • brain tumour
  • intracranial aneurysm
  • trauma
163
Q

What are the classic cerebellar signs (DANISH)?

A
  • D: dysdiadochokinesia
  • A: ataxia
  • N: nystagmus
  • I: intentional tremor
  • S: slurred speech
  • H: hypotonia
164
Q

What is Charcot-Marie-Tooth disease?

A
  • autosomal dominant disease affecting peripheral motor and sensory nerves
  • cause dysfunction in myelin and axons
165
Q

What are classical presentations of Charcot-Marie-Tooth disease?

A
  • high foot arches (pes cavus)
  • distal muscle wasting (stork calves)
  • lower leg and hand weakness
  • reduced tendon reflexes and sensory tone
166
Q

What are the causes of peripheral neuropathy?

A
  • Alcohol
  • B12 deficiency
  • Cancer and CKD
  • Diabetes and drugs (isoniazid, amiodarone and cisplatin)
  • Every vasculitis
167
Q

How is Duchenne’s muscular dystrophy passed down and who does it affect?

A
  • X-linked recessive mutation
  • boys affected exclusively
168
Q

What is the pathophysiology and presentation of Duchenne’s muscular dystrophy?

A
  • muscle is replaced with adipose tissue
  • causes difficulty getting up from lying down
  • skeletal deformities: scoliosis, hyperlordosis
169
Q

What is carpal tunnel syndrome?

A
  • compression of the medial nerve as it travels through the wrist
170
Q

What is the anatomy of the carpal tunnel?

A
  • between the carpal bones and flexor retinaculum
  • flexor retinaculum: runs across palmar side of wrist
  • median nerve and flexor tendons travel through
171
Q

Which muscles does the median nerve provide motor function to and which branch is it?

A
  • abductor pollicis brevis
  • opponens pollicis
  • flexor pollicis brevis
  • palmar digital cutaneous branch
172
Q

What does the palmar cutaneous branch innervate?

A
  • sensory to palm
  • thumb
  • index and middle finger
  • lateral half of ring finger
173
Q

What are the risk factors for carpal tunnel syndrome?

A
  • repetitive strain
  • obesity
  • perimenopause
  • RA
  • diabetes
174
Q

How does carpal tunnel syndrome present?

A
  • worse at night
  • sensory symptoms: numbness, paraesthesia, burning, pain
  • weakness of thumb movements, grip strength, difficulty with fine movement, wasting of thenar muscles
175
Q

What is Phalen’s test?

A
  • fully flexing the wrist and holding it there
  • wrists bent inwards at 90º
  • triggers numbness and parasthesia
176
Q

What is Tinel’s test?

A
  • tapping the wrist where the median nerve meets the carpal tunnel
  • triggers numbness and parasthesia
177
Q

What other investigations are done for carpal tunnel syndrome?

A
  • nerve conduction studies
  • carpal tunnel questionnaire
178
Q

How is carpal tunnel syndrome managed?

A
  • rest and altered activities
  • wrist splints
  • steroid injections
  • surgery: flexor retinaculum cut to relieve pressure
179
Q

What occurs in the frontal lobe?

A
  • voluntary and planned motor behaviours
  • motor speech area (Broca’s)
  • personality
  • planning
180
Q

What is the function of the temporal lobe?

A
  • hearing
  • language comprehension
  • semantic knowledge
  • memory
  • emotional behaviour
181
Q

What is Alzheimer’s disease?

A
  • leading cause of dementia
  • progressive neurodegenerative disorder causing deterioration in mental performance
  • general atrophy of brain
  • frontal and temporal lobes affected in particular
182
Q

What is the presentation of Alzheimer’s?

A
  • temporal: episodic memory disorder
  • parietal: visuospatial difficulties
  • receptive and expressive dysphagia
  • emotional disorder/psychosis
  • problems with planning and problem solving
  • early loss of language (subtle)
183
Q

What is the pathophysiology of Alzheimer’s disease?

A
  • accumulation of β-amyloid peptides > plaques
  • degrades amyloid precursor protein
  • leads to neuronal damage, neurofibrillary tangles, amyloid plaques
  • loss of Ach
184
Q

Which areas of the brain are most affected by Alzheimer’s?

A
  • hippocampus
  • amygdala
  • temporal neocortex
  • subcortical nuclei
185
Q

What are the risk factors for Alzheimer’s?

A
  • 1st degree relative
  • Down’s
  • depression/loneliness
  • decreased exercise, physical activity
186
Q

What are β-amyloid plaques?

A
  • excess deposition of β-amyloid
  • amyloid precursor protein broken down (found in cell membrane of neurones)
  • accumulate between synapses and affect nerve transmission
  • cause localised inflammation
187
Q

What is the management of dementia?

A
  • AChE inhibitors: donepezil: inc cholinergic transmission in brain
  • NMDA antagonists: inhibits glutamate receptors
  • antipsychotics
188
Q

What is fronto-temporal dementia?

A
  • frontal and temporal lobe atrophy: loss of spindle neurones
  • behaviour change
  • disinhibition and emotional unconcern
189
Q

How is dementia investigated?

A
  • CT/MRI to look for lesions/atrophy
  • bloods
  • questionnaires: 6 CIT
190
Q

What is syncope?

A
  • temporarily losing consciousness
  • due to disruption of blood flow to brain
  • also called vasovagal episodes or fainting
191
Q

What is the presentation of syncope?

A
  • hot and clammy, sweaty
  • heavy
  • dizzy, lightheaded
  • vision going dark
192
Q

What are the primary causes of syncope?

A
  • dehydration
  • missed meals
  • extended standing
  • vasovagal response to stimuli: surprise, pain
193
Q

What are the secondary causes of syncope?

A
  • hypoglycaemia
  • dehydration
  • anaemia
  • infection
  • anaphylaxis
  • arrhythmia
194
Q

What investigations are done for syncope?

A
  • ECG/24 hr ECG
  • echocardiogram
  • bloods: FBC, electrolytes, blood glucose
195
Q

What are some causes of lower motor neurone injury?

A
  • MND, spinal muscular atrophy, polio
  • Guillain Barre
  • neuropathies
  • myasthenia gravis
  • myositis
196
Q

What is the presentation of spinal muscular atrophy?

A
  • symmetrical, proximal muscle weakness caused by loss of motor neurons
  • lower limbs more affected than upper
  • affects bulbar function and breathing
197
Q

Describe SMA 1 and 2

A
  • SMA 1: onset in first few months, death within 2 years
  • SMA 2: onset in 18 months, never walk but survive to adulthood
198
Q

Describe SMA 3 and 4

A
  • SMA 3: onset after 1y/o, walk but later lose ability, resp affected
  • SMA 4: onset in 20s, ability to walk for short distances, everyday tasks > fatigue. resp + life expectancy not affected
199
Q

What is the pathophysiology behind neuropathies?

A
  • primary demyelination > secondary axonal degeneration
  • primary axonal degeneration > secondary demyelination
200
Q

What are the types of peripheral neuropathies?

A
  • mononeuropathy: one nerve
  • mononeuropathy multiplex: several nerves, no pattern
  • polyneuropathy: many nerves (distal + symmetrical)
201
Q

What is Lambert Eaton syndrome?

A
  • autoimmunity against presynaptic Ca channels in NMJ
  • symptoms improve with exertion
  • associated with small cell lung carcinoma
  • symptoms start with extremities
202
Q

What is the presentation of Lambert Eaton syndrome?

A
  • proximal muscle weakness
  • diplopia
  • ptosis
  • dysphagia
203
Q

What is the treatment of Lambert Eaton syndrome?

A
  • Amifampridine
  • immunosuppressants: prednisolone
204
Q

How can you differentiate between UMN and LMN lesions?

A
  • forehead spared in UMN
  • ask patient to raise eyebrows
  • if can move both sides then UMN lesion
  • if one side affected then LMN lesion
205
Q

What is the presentation of a radial nerve palsy and what are the nerve roots?

A
  • roots C5-T1
  • wrist drop
  • innervates extensor muscles
206
Q

What is the presentation of a ulnar nerve palsy and what are the nerve roots?

A
  • roots C8 + T1
  • claw hand (4th and 5th fingers)
207
Q

What are differential diagnoses for epilepsy?

A
  • syncope
  • cardiac arrhythmia
  • panic attack
  • non-epileptic + dissociative seizures
  • TIA
  • migraine
208
Q

What is Brown-Sequard syndrome?

A
  • hemisection of the spinal cord
  • involves anterolateral system and DCML pathway
  • symptoms occur below the lesion
209
Q

What are the symptoms of Brown-Sequard?

A
  • contralateral loss of pain and temperature
  • ipsilateral loss of proprioception and vibration
  • ipsilateral UMN weakness below lesion
210
Q

Describe GCS?

A
  • Eyes, verbal response, motor response
  • max score is 15, min is 3
  • 8/15 or below: secure airway

Osha 2a (15 decks)

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