My Neurology

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  1. What are the main causes of ICU admission due to altered consciousness?
    • Faint
    • Fit
    • Funny turn (meabolic/traumatic/psychiatric cause)
  2. What important aspects of a history are needed when investigating altered consciousness in general?
    • Patient's opinion: Feeling before/after and during
    • Witness opinion: What happened before/after/during
    • Risk factors for epilepsy
    • Past history
  3. Describe an attack of syncope
    • Commonly related to a trigger
    • Prodromes always present
    • Gradual onset (dizziness, loss of vision) but short duration and rapid recovery
    • Convulsive jerks can occur
    • Incontinence/tongue biting uncommon
    • No confusion afterwards
  4. Describe a seizure
    • Triggers rare
    • Prodromes common
    • Sudden onset
    • 1-3 minute duration
    • Jerks frequent and prolonged
    • Incontinence/tongue biting uncommon
    • Confusion/amnesia afterward with slow recovery
  5. Outline the pathogenesis and classification of a seizure
    • A sustained and synchronised cortical discharge, causing an excitation/inhibition imbalance
    • Generalised tonic-clonic: potential amplitude/frequency steadily decrease causing tonic (rigid collapse) and clonic (twitching) stages
    • Partial: Loss of awareness or cortical phenomena
  6. What investigations are use to explore a suspected seizure?
    • ECG: Always given after any blackout
    • Blood glucose: Hypoglycaemia common cause of collapse
    • MRI/CT: Rule out many mimicking or causative diseases
    • EEG: Used for prognosis after seizure diagnosed
  7. How is a seizure managed?
    • Risk factors assessed uding EEG and CT/MRI
    • Treatment not usually given unless risk of another seizure is above 60% (generally after 2 seizures)
    • Localised seizures: Lamotrigine, carbamazepine
    • Generalised seizures: Valproate
  8. Define status epilepticus
    • Either:
    • A seizure which carries on for 30 minutes or more
    • A series of seizures with no regaining of consciousness in between them
  9. How is status epilepticus treated?
    • First aid
    • Benzodiazepines: Relax muscles, but can only be used twice
    • Phenytoin: Antiepileptic which stabilises voltage-gated sodium channels in inactive state = suppressed brain activity
  10. Define epilepsy and its classification
    • Epilepsy is the tendency to have recurrent, unprovoked seizures
    • Localised onset: Begin in an area of abnormality with the rest of the brain normal
    • Generalised onset: Usually genetic/congenital neurotransmitter imbalance
  11. Describe the economic burden of stroke
    • 3rd most common cause of death
    • Frequent cause of disability
    • Consumes 5% of the NHS budget
  12. Define stroke
    Rapidly developing clinical signs of focal/global disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than a vascular one
  13. Describe the different pathogeneses of stroke
    • Ischaemic: 80% of cases - reduce blood flow from blockage/hypoperfusion
    • Intra-cerebral haemorrhage: 15-20%, small vessels perpendicular to the MCAs rupture in hypertension
    • Lacunar: Small perforating arteries (supply basal ganglia) rupture/stenose in hypertension
  14. Outline the mechanisms of neurone death in ischaemia
    • Excitotoxicity: Loss of ATP causes reduction in K/NA pump action = potassium exits/sodium enters = H20 entry and swelling
    • Glutamate: Released due to potassium exit = increased calcium = protease activation = apoptosis
    • Inflammation: Causes infiltration/cell death
  15. Describe the geography of a stroke
    • Core: Main affected area, with unsalvageable necrotic tissue
    • Penumbra: Halo of semi-ischaemic tissue, salveagable with emergency treatment
    • Oligaemia: Very slightly ischaemic area
  16. What is a TACS and how does it present?
    • Total anterior circulation stroke; damages one anterior hemisphere e.g. MCA occlusion
    • Presents with:
    • Contralateral hemiparesis
    • Homonymous hemianopia
    • Higher dysfunction (aphasia, memory loss, agnosia)
  17. What is a PACS, LACS and PCS?
    • PACS: Partial anterior circulation stroke; 2/3 of TACS clinical features
    • LACS: Lacunar ACS, affects small area with features varying
    • PCS: Posterior circulation stroke; affects CNs, stem or cerebellum
  18. What are the features of cerebellar infarction?
    • DANISH:
    • Disdiadochokinesis
    • Ataxia
    • Nystagmus
    • Intention tremor
    • Slurred speech
    • Hypotonia
  19. What other diseases can mimic stroke?
    • Seizure
    • Hypoglycaemia
    • Infection
    • Toxic-metabolic
    • Neoplasia
    • Syncope/CV disease
  20. How is a stroke diagnosed?
    • Acute rise in BP (maintains CPP)
    • Neuro exam
    • ECG for AF, IE
    • Bloods: Obs, coag, FBC, U+Es, lipids, glucose
    • Imaging: CT/MRI for space occupying lesion
  21. How is stroke managed acutely?
    • After BP, BM and coagulation screen performed, transferred
    • Thrombolysis given within 'window'; 4.5 hours
    • Carotid endartrectomy if stenosis
  22. What are the contraindications for thrombolysis in stroke?
    • Previous IC bleed
    • Uncontrolled hypertension
    • Known vascular structure lesions
    • Facial trauma <3 months
  23. What is the aetiology of stroke?
    • Increasing age
    • Hypertension
    • Heart disease (especially AF, MI)
    • Smoking
    • Diabetes
    • Hypercholesterolaemia
    • Previous stroke/TIA
    • Family history
  24. Outline the mild and severe presentation of traumatic brain injury
    • Mild: Stunned for seconds/minutes, with no amnesia and a possible headache
    • Serious: Increased duration of unconsciousness, amnesia, GCS below 5 for >24 hours implies very serious, long recovery
  25. What are the sequelae and complications of traumatic brain injury?
    • Cognitive impairment in incomplete recovery
    • Post traumatic epilepsy
    • Post traumatic syndrome; malasise, headache etc
    • Hydrocephalus
    • Chronic subdural haematoma
  26. How is acute traumatic brain injury managed?
    • Airway maintenance/ventilation,
    • CT imaging if haematoma/fracture
    • Bloods for FBC, biochemistry and clotting
    • ICP monitoring
  27. Outline some clinical features of sub-arachnoid haemorrhage
    • Sudden, severe occipital heachache
    • Vomiting
    • Neck stiffness
    • Kernig's sign (meningism)
    • Coma
    • Important to differentiate from migraine
  28. How is a SAH managed?
    • Bed rest
    • Supportive measures, e.g. ventilation
    • Hypertension control
    • Dexamethasone (reduces cerebral oedema)
    • Nimodipine (CCB; prevents vasospasm)
  29. What aspects of a history are important when investigating a headache?
    • Site: Tension headache quite superficial
    • Onset: Age
    • Character: throbbing/crushing/pulsatile
    • Radiation
    • Associated: photophobia/prodromes/nausea
    • Timing: Time till maximal symptoms present
    • Exac/reliev: Triggers, e.g. posture, cough, alcohol
    • Severity: 1-10
    • Family history/medication/social history
  30. What red flags are important in headaches?
    • Age over 50
    • Thunderclap
    • Focal/non-focal deficit
    • Posture changes (high/low CSF)
    • Early morning headaches
    • Systemic symptoms
    • Seizures/meningism
    • Temporal artery tenderness/jaw claudication
    • Past history of disease
  31. Outline features to be examined in a headache
    • GCS
    • BP/pulse
    • Pyrexia
    • Meningism
    • Skin rash
    • Temporal artery tenderness
    • CN tests
  32. Describe the characteristics of a raised pressure headache
    • Worse when lying flat, improved when sitting/standing
    • Worse in morning
    • Persistent nausea/vomiting
    • Worse on valsalva (try to breath when airway closed)
    • Worse with physical exertion
    • Transient visual changes when posture change
  33. What are the causes and clinical findings of raised pressure headaches?
    • Causes: Mass effect, increases venous pressure, CSF obstruction, ideopathic
    • Examination: Papilloedema, CN dysfunction, focal neurological signs
  34. What are the characteristics and causes of low pressure headaches?
    • Characteristics: Headache worse on sitting/standing, relieved by lying flat, due to loss of volume and pressure on CNs, veins/meninges
    • Causes: Lumbar punctures, spontaneous intracranial hypotension
  35. Define migraine and its pathogenesis
    • Neurovascular disorder caused by primary dysfunction in brainstem sensory nuclei, with vascular changes occuring due to neural activation
    • Pain results from pain-sensitive cranial blood vessels and the trigeminal fibres that innervate them
  36. What are the characteristics of a migraina
    • Triggers: Hormones, weather, stress, sleep disturbance
    • Associated features: With/without aura, pro and post-dromes occur sometimes days from onset
  37. How are migraines managed?
    • Lifestyle: Trigger avoidance, e.g. reduce caffeine, regular sleep/meals
    • Medical: Simple analgesia, triptans and antiemetics
    • Prophylaxis: Beta blockers, tricyclic anti-depressants, anti-epileptics
  38. What is a thunderclap headache?
    • Abrupt onset of severe headache which reaches maximal intensity in under 5 minutes (usually less than 30seconds)
    • Sub arachnoid haemorrhage unless proven otherwise
  39. How are thunderclap headaches investigated?
    • Routine bloods/cultures
    • ECG
    • Urgent CT (blood visible in most SAHs)
    • Lumbar puncture for xanthochromia if CT negative; RBCs degrade in CSF
  40. Outline the pathogenesis of MS
    • CD4 T cell mediated inflammatory process
    • Occurs in the white matter of the brain and spinal cord
    • Inflammatory cell infiltration, myelin degredation and phagocytosis
  41. What are the pathological characteristics of MS?
    • Multiple plaques of demyelination within the brain and spinal cord
    • Plaques disseminated in space and time
    • Especially found in optic nerves, brainstem, cerebellum, pyramidal tracts
    • Focal inflammation
    • Permanent axonal destruction
  42. What are the clinical features of MS, concerning optic, brainstem an cord lesions?
    • Optic: Acute, unilateral blurred vision. Pain
    • Brainstem: Diplopia, vertigo, nystagmus, numbness, dysarthria/dysphagia
    • Cord: Progressive spastic paraparesis, Lhermitte's sign, incontinence, paraesthesia/numbness
  43. What investigations are useful in MS?
    • MRI: Multifocal plaques; elliptical bordered lesions with no mass effect
    • Lumbar puncture: Oligoclonal IgG and raised CSF mononuclear cells (infiltration)
    • VERS: Visual evoked responses, shows optic neuropathy
  44. List the types of MS
    • Relapsing remitting: >2 neurological disturbances over 2-3 years, with some recovery
    • Primary progressive: Only progression, no relapse
    • Secondary progressive: Only progression, no relapse, develops from R/R
    • Progressive relapsing: Steady progression with superimposed R/R
  45. What is the differential diagnosis in suspected MS?
    • Lime disease
    • Stroke
    • Nerve impingement
    • Guillian Barre
    • Vitamin deficiency
    • Diabetes
    • Vasculitides
  46. How is MS managed acutely?
    • Short courses of steroids, e.g. IV methylprednisolone with a PPI
    • Only decreases severity/length of relapses
    • High dose (1g daily for 3 days
  47. What treatments for MS are available, apart from steroids?
    • Beta interferon: Reduces relapse rate and lesion formation
    • Immunosuppresants: Azathioprine, cyclophosphamide
    • Natalizumab: Anti leucocyte antibody, preventing CNS migration
    • Intensive physiotherapy/occupational therapy
  48. What pathological changes are seen in Parkinsons?
    • Progressive degeneration of substantia nigra
    • Lewy bodies develop; spherical masses which displace cell components (cortical = dementia, brain stem = parkinsons)
  49. Explain the common clinical features of parkinsons
    • Directly related to pathways which connect to basal ganglia
    • Motor: Tremor
    • Oculo-motor: Reduced ocular pursuit
    • Associative/Limbic: memory loss
    • Orbitofrontal: Executive dysfunction
  50. What are the common clinical features of Parkinsons?
    • Progressive degeneration, over months or years
    • Motor: Tremor, especially at rest. Rigidity. Bradykinesia. Instability
    • Neuropsychiatric: Executive dysfunction, slowed cognitive speed, memory loss, sleep disturbance
    • Autonomic: Orthostatic hypotension, hyperhidrosis, constipation
  51. What are the causes of Parkinsonian syndrome?
    • Parkinsons
    • Alzhiemers
    • Multiple cerebral infarction
    • Drugs
    • Supranuclear palsy
  52. What are the criteria for diagnosing Parkinsons?
    • 1 of: Muscular rigidity; pill rolling tremor; postural instability
    • 3 of: Unilateral onset; rest tremor; persistent asymmetry; >10yr onset; improvement on levadopa OR levadopa chorea
  53. What features of a history suggest a different cause of Parkinsonian syndrome than Parkinsons?
    • Repeated strokes
    • Repeated head trauma
    • Encephalitis
    • More than one affected relative
    • Cerebellar signs
  54. List the first line drugs in Parkinsons
    • L-DOPA; Dopamine precursor - severe chorea/adverse effects
    • Dopamine agonist
    • MAO B inhibitors
    • COMT inhibitors; later disease - COMT degrades neurotransmitters
Card Set:
My Neurology
2012-02-02 21:08:24
seizures stroke degenerative disease

seizures, stroke, degenerative disease
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