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What are the main causes of ICU admission due to altered consciousness?
- Funny turn (meabolic/traumatic/psychiatric cause)
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
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
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
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
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
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
Define status epilepticus
- A seizure which carries on for 30 minutes or more
- A series of seizures with no regaining of consciousness in between them
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
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
Describe the economic burden of stroke
- 3rd most common cause of death
- Frequent cause of disability
- Consumes 5% of the NHS budget
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
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
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
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
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)
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
What are the features of cerebellar infarction?
- Intention tremor
- Slurred speech
What other diseases can mimic stroke?
- Syncope/CV disease
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
How is stroke managed acutely?
- After BP, BM and coagulation screen performed, transferred
- Thrombolysis given within 'window'; 4.5 hours
- Carotid endartrectomy if stenosis
What are the contraindications for thrombolysis in stroke?
- Previous IC bleed
- Uncontrolled hypertension
- Known vascular structure lesions
- Facial trauma <3 months
What is the aetiology of stroke?
- Increasing age
- Heart disease (especially AF, MI)
- Previous stroke/TIA
- Family history
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
What are the sequelae and complications of traumatic brain injury?
- Cognitive impairment in incomplete recovery
- Post traumatic epilepsy
- Post traumatic syndrome; malasise, headache etc
- Chronic subdural haematoma
How is acute traumatic brain injury managed?
- Airway maintenance/ventilation,
- CT imaging if haematoma/fracture
- Bloods for FBC, biochemistry and clotting
- ICP monitoring
Outline some clinical features of sub-arachnoid haemorrhage
- Sudden, severe occipital heachache
- Neck stiffness
- Kernig's sign (meningism)
- Important to differentiate from migraine
How is a SAH managed?
- Bed rest
- Supportive measures, e.g. ventilation
- Hypertension control
- Dexamethasone (reduces cerebral oedema)
- Nimodipine (CCB; prevents vasospasm)
What aspects of a history are important when investigating a headache?
- Site: Tension headache quite superficial
- Onset: Age
- Character: throbbing/crushing/pulsatile
- 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
What red flags are important in headaches?
- Age over 50
- Focal/non-focal deficit
- Posture changes (high/low CSF)
- Early morning headaches
- Systemic symptoms
- Temporal artery tenderness/jaw claudication
- Past history of disease
Outline features to be examined in a headache
- Skin rash
- Temporal artery tenderness
- CN tests
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
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
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
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
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
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
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
How are thunderclap headaches investigated?
- Routine bloods/cultures
- Urgent CT (blood visible in most SAHs)
- Lumbar puncture for xanthochromia if CT negative; RBCs degrade in CSF
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
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
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
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
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
What is the differential diagnosis in suspected MS?
- Lime disease
- Nerve impingement
- Guillian Barre
- Vitamin deficiency
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
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
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)
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
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
What are the causes of Parkinsonian syndrome?
- Multiple cerebral infarction
- Supranuclear palsy
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
What features of a history suggest a different cause of Parkinsonian syndrome than Parkinsons?
- Repeated strokes
- Repeated head trauma
- More than one affected relative
- Cerebellar signs
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