Card Set Information
seizures stroke degenerative disease
seizures, stroke, degenerative disease
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?
: Feeling before/after and during
: What happened before/after/during
Risk factors for epilepsy
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
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
: potential amplitude/frequency steadily decrease causing tonic (rigid collapse) and clonic (twitching) stages
: Loss of awareness or cortical phenomena
What investigations are use to explore a suspected seizure?
: Always given after any blackout
: Hypoglycaemia common cause of collapse
: Rule out many mimicking or causative diseases
: 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)
: Lamotrigine, carbamazepine
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?
: Relax muscles, but can only be used twice
: 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
: Begin in an area of abnormality with the rest of the brain normal
: 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
: 80% of cases - reduce blood flow from blockage/hypoperfusion
: 15-20%, small vessels perpendicular to the MCAs rupture in hypertension
: Small perforating arteries (supply basal ganglia) rupture/stenose in hypertension
Outline the mechanisms of neurone death in ischaemia
: Loss of ATP causes reduction in K/NA pump action = potassium exits/sodium enters = H20 entry and swelling
: Released due to potassium exit = increased calcium = protease activation = apoptosis
: Causes infiltration/cell death
Describe the geography of a stroke
: Main affected area, with unsalvageable necrotic tissue
: Halo of semi-ischaemic tissue, salveagable with emergency treatment
: 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
Higher dysfunction (aphasia, memory loss, agnosia)
What is a PACS, LACS and PCS?
: Partial anterior circulation stroke; 2/3 of TACS clinical features
: Lacunar ACS, affects small area with features varying
: Posterior circulation stroke; affects CNs, stem or cerebellum
What are the features of cerebellar infarction?
What other diseases can mimic stroke?
How is a stroke diagnosed?
Acute rise in BP (maintains CPP)
ECG for AF, IE
: Obs, coag, FBC, U+Es, lipids, glucose
: 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
Known vascular structure lesions
Facial trauma <3 months
What is the aetiology of stroke?
Heart disease (especially AF, MI)
Outline the mild and severe presentation of traumatic brain injury
: Stunned for seconds/minutes, with no amnesia and a possible headache
: 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?
CT imaging if haematoma/fracture
Bloods for FBC, biochemistry and clotting
Outline some clinical features of sub-arachnoid haemorrhage
Sudden, severe occipital heachache
Kernig's sign (meningism)
Important to differentiate from migraine
How is a SAH managed?
Supportive measures, e.g. ventilation
Dexamethasone (reduces cerebral oedema)
Nimodipine (CCB; prevents vasospasm)
What aspects of a history are important when investigating a headache?
: Tension headache quite superficial
: Time till maximal symptoms present
: Triggers, e.g. posture, cough, alcohol
Family history/medication/social history
What red flags are important in headaches?
Age over 50
Posture changes (high/low CSF)
Early morning headaches
Temporal artery tenderness/jaw claudication
Past history of disease
Outline features to be examined in a headache
Temporal artery tenderness
Describe the characteristics of a raised pressure headache
Worse when lying flat, improved when sitting/standing
Worse in morning
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?
: Mass effect, increases venous pressure, CSF obstruction, ideopathic
: Papilloedema, CN dysfunction, focal neurological signs
What are the characteristics and causes of low pressure headaches?
: Headache worse on sitting/standing, relieved by lying flat, due to loss of volume and pressure on CNs, veins/meninges
: 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
: Hormones, weather, stress, sleep disturbance
: With/without aura, pro and post-dromes occur sometimes days from onset
How are migraines managed?
: Trigger avoidance, e.g. reduce caffeine, regular sleep/meals
: Simple analgesia, triptans and antiemetics
: 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?
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
Permanent axonal destruction
What are the clinical features of MS, concerning optic, brainstem an cord lesions?
: Acute, unilateral blurred vision. Pain
: Diplopia, vertigo, nystagmus, numbness, dysarthria/dysphagia
: Progressive spastic paraparesis, Lhermitte's sign, incontinence, paraesthesia/numbness
What investigations are useful in MS?
: Multifocal plaques; elliptical bordered lesions with no mass effect
: Oligoclonal IgG and raised CSF mononuclear cells (infiltration)
: Visual evoked responses, shows optic neuropathy
List the types of MS
: >2 neurological disturbances over 2-3 years, with some recovery
: Only progression, no relapse
: Only progression, no relapse, develops from R/R
: Steady progression with superimposed R/R
What is the differential diagnosis in suspected MS?
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?
: Reduces relapse rate and lesion formation
: Azathioprine, cyclophosphamide
: 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
: Reduced ocular pursuit
: memory loss
: Executive dysfunction
What are the common clinical features of Parkinsons?
Progressive degeneration, over months or years
: Tremor, especially at rest. Rigidity. Bradykinesia. Instability
: Executive dysfunction, slowed cognitive speed, memory loss, sleep disturbance
: Orthostatic hypotension, hyperhidrosis, constipation
What are the causes of Parkinsonian syndrome?
Multiple cerebral infarction
What are the criteria for diagnosing Parkinsons?
: Muscular rigidity; pill rolling tremor; postural instability
: 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 head trauma
More than one affected relative
List the first line drugs in Parkinsons
L-DOPA; Dopamine precursor - severe chorea/adverse effects
MAO B inhibitors
COMT inhibitors; later disease - COMT degrades neurotransmitters