MED627 - Cerebrovascular Disease and Disorders of Consciousness Flashcards
Define transient loss of consciousness
- Spontaneous LOC with complete recovery
- TLOC/blackout/syncope
Describe the epidemiology of TLOC
- Increases with age
- Increase in incidence rate was steeper starting at 70yrs
- Rates similar among men and women
- Survival worst for patients with cardiovascular disease
What are the clinical challenges of TLOC?
- Main witness unconscious
- Eyewitness account unreliable but essential
- Unpredictable, hence difficult to record
- Occasionally life threatening
- Driving restrictions, health and safety
- Initial diagnosis often inaccurate - Results in a delay
What are the risks of TLOC?
Can be the first symptom of fatal arrhythmia - >100,000 deaths every year in the UK
Sudden deaths often attributed to cardiac arrhythmias - Inherited cardiomyopathies in people under the age of 30
Syncope may result in injuries to patients or others as a result of accidents
Name some differentials of TLOC
Neurally mediated (reflex) syncope
o Vasovagal
o Situational – cough/micturition
o Carotid sinus hypersensitivity
Cardiac syncope
Neurological o Epilepsy o Sleep disorders o Raised ICP o Psychogenic non epileptic attacks
Orthostatic hypotension
o Drugs
o Neurodegenerative disorders
Metabolic disorders
What would you include in a history following a TLOC?
Before the attack o Any warning? – typical aura o Any provoking features o Associated symptoms o In what circumstances the attacks occur o Can the attacks be prevented?
During the attack o Actual LOC o Duration of attack o Change in complexion o Verbal/tactile responsiveness o Movement/limb jerking o Injuries o Pulse o (Tongue biting and urine incontinence) – only indicative of epilepsy if very severe
After an attack o Recovery – rapid/prolonged o Confused or sleepy o The duration o How much does the patient remember? o (muscle pain)
Frequency
Describe vasovagal syncope
- No comprehensive theory for vasovagal syncope
- 0.5% of the population faint per annum (women>men)
- 1:200 referrals to A&E
- 75,000 attendances per annum in UK
- Posture, provocation, prodromal
- Convulsive movements common
- Diagnosis depends on history
- Lack of post-ictal confusion, hearing people around you before you can respond and recurrence of blackout on regaining upright posture helpful in diagnosis
- Common sense
Describe micturition syncope
- Fainting shortly after or during urination
- Micturition involves relaxation, not straining unless (male patient) has an enlarged prostate or stricture
- Role of pelvic venous plexus
Describe cardiac syncope and give an example
- Temporary but sudden reduction in blood supply and hence oxygen to the brain as a result of cardiovascular conditions
- The temporary but sudden reduction in blood supply triggering syncope is caused by vasodilation, hypotension, arrhythmia
- The onset of syncope is relatively rapid and recovery from LOC is spontaneous, complete and usually prompt
- E.g. Long QT syndrome
What suggests epilepsy as the underlying cause of TLOC?
- Description of an aura - Patient normally finds it difficult to describe
- Brief attack
- Prolonged post ictal confusion
- Head turning or posturing of body
- Stiffening of body and myoclonic jerking (not oscillation)
- Abnormal behaviour of which patients do not remember
- Severe tongue biting
What suggests a diagnosis of NEAD in a history? And what suggests a diagnosis of epilepsy?
NEAD o Scant description from patient o Frequent or long seizures o Different types of seizures o Crying during recovery
Epilepsy o Injury o Tongue biting o Incontinence o Seizures in sleep
Describe NEAD
- Common – more likely to witness NEAD than an epileptic seizure
- Gradual onset, undulating motor activity with pauses
- Sinusoidal and asynchronous arm and leg movements
- Prolonged atonia, rhythmic pelvic movements, side to side head movements
- Post ictal crying, high anxiety in carers
- Prolonged attack with prolonged/unexpected sudden recovery
How do you make of a diagnosis of NEAD?
o Description/nature of seizure changes with time – good documentation
o Unusually frequent, drug-unresponsive seizures, sometimes provoked by stress
o History of somatoform/multiple unexplained symptoms, multiple surgical procedures
o History of personality disorder, alcohol abuse, self har, parasuicide, childhood abuse, psychiatric treatment
o Video the attack
What are the risks of misdiagnosing NEAD?
o Inappropriate treatment – risk of adverse effects of anti-epileptic drugs, including teratogenicity
o Ineffective treatment – when there is an effective treatment
o Reinforcement of abnormal illness behaviour
Evolution of functional symptoms
Incapacity
Financial and social dependency
What are some suitable investigations following a TLOC?
ECG
o Rule out cardiac causes
o Always do it
EEG
o Not normally used to distinguish epilepsy from other TLOC
o Non-specific abnormalities common
o Very useful if it captures the event
Neuroimaging
o Not normally used to distinguish epilepsy from other TLOC
o Nonspecific and co-incidental abnormalities common
Define seizure
the clinical manifestation of an abnormal, excessive excitation and synchronization of a population of cortical neurons
Define epilepsy
a tendency to recurrent seizures >24hrs apart which are not provoked by systemic or acute neurologic insults
What is an EEG?
- Electroencephalography
- Records cortical electrical activity – usually from the scalp
- Most important neurophysiological study for the diagnosis, prognosis, and treatment of epilepsy
- Electrodes usually attached in the 10/20 system
Briefly describe the 1981 ILAE classification of seizures
Partial
- Simple partial
- Complex partial
- Secondarily generalised
Generalised
- Absence
- Myoclonic
- Atonic
- Tonic
- Tonic-clonic
Describe absence seizures
- Type of generalised seizure
- Brief staring spells with impairment of awareness
- 3-20 seconds
- Sudden onset and sudden resolution
- Often provoked by hyperventilation
- Onset typically between 4 and 14 years of age, and resolve by age 18
- Normal development and intelligence
What EEG finding would be seen during an absence seizure?
Generalised 3 Hz spike-wave discharges
Describe myoclonic seizures
- Generalised
- Brief, shock-like jerk of a muscle or group of muscle
- Differentiate from benign, non-epileptic myoclonus (e.g. when falling asleep)
What EEG finding would be seen during a myoclonic seizure?
Generalised 4-6 Hz polyspike-wave discharges
Describe tonic seizures
- Symmetric, tonic muscle contraction of extremities with tonic flexion of waist and neck
- Not the same as the tonic phase of a tonic clonic seizures
- Duration – 2-20 seconds
What EEG finding would be seen during a tonic seizure?
Sudden attenuation with generalised, low-voltage fast activity (most common) or generalised polyspike-wave
Describe atonic seizures
- Sudden loss of postural tone
- When severe often results in falls
- When milder produces head nods or jaw drops
What EEG finding would be seen during a atonic seizure?
Sudden diffuse attenuation or generalised-polyspike wave
Described generalised tonic clonic seizures
- Associated with loss of consciousness and post-ictal confusion/lethargy
- Duration – 30-120 seconds
- Tonic phase – stiffening and fall, often associated with ictal cry (caused by stiffening of pharynx muscles
- Clonic phase – rhythmic extremity jerking
What EEG finding would be seen during a generalised tonic-clonic seizure?
generalised polyspikes
Describe simple partial seizures
- Same thing as an aura
- Patient aware throughout
- Diverse range, leading to diagnostic challenges
- Symptoms depend on where in the brain is affected
o Somatosensory
o Motor
o Visual/ auditory/ olfactory
o Autonomic sensations
o Psychic/ experiential
o Clonic seizure - Seizure always the same for the patient – it does not change from seizure to seizure
- Patients usually struggle to describe what happens
Describe complex partial seizures
- Impaired consciousness – loss of awareness
- Clinical manifestations vary with site of origin and degree of spread
o Presence and nature of aura
o Automatisms – semi purposeful movement
o Other motor activity - Duration typically <2 minutes
Describe secondary generalised tonic clonic seizures
- Begins focally, with or without focal neurological symptoms
- Tonic and clonic phases with variable symmetry, typical duration 1-3 minutes
- Post ictal confusion
- Can have transient focal deficit after seizure – Todd’s paresis
What are epilepsy syndromes?
- Grouping of patients that share similar o Seizure types o Age of onset o Natural history/prognosis o EEG patterns o Aetiology/ Genetics
What are epilepsy syndromes divided in to?
o Idiopathic – when the disorder was not associated with other neurological or neuropsychological abnormalities
o Symptomatic – when there was a neurological or neuropsychological abnormality, and the cause was known
o Cryptogenic – when there was a neurological or neuropsychological abnormality and the cause was unknown
Describe temporal lobe epilepsy
- Common – temporal lobe most common location for localised seizure
- Onset at any age
- EEG shows temporal lobe epileptiform discharges
o EEG changes when seizure not occurring
o Not always seen - Simple partial, complex partial and secondary GTCS
- May be symptomatic or cryptogenic
- Hippocampus sclerosis can be a cause
Describe juvenile myoclonic epilepsy
- Juvenile onset
- Myoclonic seizures, brief subtle absence, GTCS
- Seizures have morning predominance, exacerbated by sleep deprivation and alcohol
- Idiopathic
o Otherwise well and neurologically intact - EEG shows generalised spike or polyspike/wave discharges
- Often photosensitive (30-40%)
Describe West syndrome
- Infantile onset
- Hypsarrhythmic EEG
- Infantile (epileptic spasms)
- Cryptogenic vs symptomatic
Describe the development of epilepsy classification in 2010
Published in epilepsia 2010
- Focal reconceptualised
o Focal epileptic seizures are conceptualised as originating within networks limited to one hemisphere
o These may be discretely localised or more widely distributed - Generalised reconceptualised
o Generalised epileptic seizures are conceptualised as originating at some point within, and rapidly engaging, bilaterally distributed networks
o Can include cortical and subcortical structures but not necessarily include the entire cortex - Introduced concept of networks
- Language and structure for organising epilepsies
What was partial, simple partial and complex partial seizures changed to under the new classification (2010)?
Focal, focal with impaired awareness (for both simple and complex)
What was secondary generalised TCS changed to under the new classification (2010)?
Focal evolving to bilateral convulsive seizure
What was cryptogenic changed to under the new classification (2010)?
Unknown
What was symptomatic changed to under the new classification (2010)?
Structural/metabolic
What was idiopathic changed to under the new classification (2010)?
Genetic
What are the rules for classifying seizures (2017)?
- Onset – Decide whether seizure onset is focal or generalised, using an 80% confidence level
- Awareness – For focal seizures, decide whether to classify by degree of awareness or to omit awareness as a classifier
- Impaired awareness at any point – a focal seizure is a focal impaired awareness seizure if awareness is impaired at any point during the seizure
- Onset predominance – classify a focal seizure by its first prominent sign or symptom but do not count transient behaviour arrest
- Behaviour arrest – A focal behavioural arrest seizure shows arrest of behaviour as the prominent feature of the entire seizure
- Motor/non-motor – a focal aware or impaired awareness seizure maybe further sub-classified by motor or non-motor characteristics. Alternatively, a focal seizure can be characterised by motor or non-motor characteristics, with specifying level of awareness.
According to the 2017 classification of seizures, what are focal seizures now divided in to? Give examples
Motor onset
- Automatisms
- Atonic
- Clonic
- Epileptic spasms
- Hyperkinetic
- Myoclonic
- Tonic
Non-motor onset
- Autonomic
- Behaviour arrest
- Cognitive
- Emotional
- sensory
Describe EEG technique
Digital + video
o Patient is filmed – useful if they have a seizure
Electrodes
o Using 19 electrodes
o Prefrontal, Frontal, temporal, occipital, central regions
o Even numbers on right side of head, odd numbers on the left, zero (Z) in midline
Name some common variable seen in EEG
Age - EEG in child is chaotic Artefacts - e.g. chewing Conscious level - e.g. sleeping, anaesthetic Drugs Cerebral pathology - e.g. cerebral palsy
Name some techniques that can be used to trigger a seizure when undertaking an EEG
Photic stimulation
o Strobe light used on patient
o If seizure triggered – photosensitive epilepsy
Hyperventilation
o Common trigger in childhood absence epilepsy
Sleep and sleep deprivation
o Sleep deprivation is known as a trigger of epilepsy
When can long-term monitoring be useful and describe the two types?
- Useful if EEG is normal but seizures persist
- Ambulatory
o EEG monitoring for 24 or 48 hours
o Takes measurements when not constricted to the examination room - Video-telemetry
o EEG, microphone and camera set up around a hospital bed
o Aim to capture 3 or more episodes to help diagnose epilepsy
What cannot an interictal EEG do?
o Exclude epilepsy
o Prove epilepsy
Describe the sensitivity of EEG
- Poor sensitivity for routine wake EEGs – only around 50% of epileptic patients will have EEG changes on their first EEG
- To increase yield
o Sleep EEG increases sensitivity (80%)
o Repeat wake and sleep EEG provides the best yield (92%) – but still not 100%
Describe the specificity of EEGs
- Specificity of EEG (correctly excluding epilepsy) is better than sensitivity at around 78-98% (Smith, 2005)
- EEG epileptiform is found in 0.5-4% of healthy adults
- BUT population is not healthy
- Other cerebral disease
o Cerebrovascular disease, migraine, cerebral palsy Alzheimer’s disease - Drugs
o Psychotropics - These factors can all cause abnormal EEGs
How is EEG useful for the classification of epilepsy?
Focal vs Generalised
o EEG can be helpful in determining whether the seizure is focal or generalised in origin
o Sometimes clinical diagnosis is difficult of focal seizures that cause a secondary generalised seizure
Syndrome identification
o Some types of epilepsies are classified into syndromes
o Use of EEG can identify a syndrome and help with specific treatment
o Inter-ictal, ictal and both
What is the role of EEG in the management of Status Epilepticus?
Convulsive
o Diagnosis if possibility of NEAD
o Monitoring of treatment if paralysed and ventilated
Non-convulsive
o Diagnosis
o Monitoring treatment
What is the role of EEG in the work up for epilepsy surgery?
- EEG vs MRI abnormality
o Does the EEG localise the seizure to the abnormality on EEG? - Epilepsy surgery only performed if high suspicion that an abnormality is the cause
- EEG can help determine this
Describe the abuses of EEG in epilepsy
- Monitoring of progress
o Not usually helpful
o EEG changes can still be present even if seizures well controlled
o More useful to take history of seizure frequency - Anti-convulsant withdrawal in adults
- Diagnosis in presence of intracerebral disease
- Diagnosis where history is of syncope
- Driving
Describe the EEG NICE guidelines
- An EEG should be performed only to support a diagnosis of epilepsy in adults in whom the clinical history suggests that the seizure is likely to be epileptic in origin
- An EEG should be performed only to support a diagnosis of epilepsy in children
o If EEG considered necessary – should be performed after the second epileptic seizure
o In certain circumstances, as evaluated by a specialist, it can be considered after a first epileptic seizure
What is rehabilitation medicine?
- The process of helping a person reach the fullest physical/psychological/social/vocational/educational potential consistent with anatomic or physiological impairment, environmental limitations and desires and life plans
- The process of active change by which a patient acquires knowledge and skills necessary for optimal physical, psychological and social function
What are some rehabilitation concepts?
- Process of education and retraining
- Disabled individual at the centre
- Interdisciplinary approach
- Goal setting is important
- Concepts of activity (disability) and participation (handicap)
- Role of personal and environmental factor
What is an acquired brain injury?
- An injury to the brain, which is not hereditary, congenital, degenerative or induced by birth trauma
- Injury to the brain that has occurred after birth
What are the types of acquired brain injury?
o Traumatic brain injury (TBI) o Haemorrhagic brain injury (HBI) o Vascular brain injury (VBI) o Anoxic (and metabolic) brain injury (ABI) o Infective brain injury (IBI)
Define TBI
- Defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force (Common data elements 2013)
Describe the epidemiology of TBI
- 1 million patients in the UK attend hospital every year
- 50% are under 16
- 275/100,000 are admitted every year
- 10-20% likely to have some long-term disability
- Physical recovery often better than cognitive or psychosocial recovery
- About 1 in 4 adults with TBI is unable to return to work 1 year after injury
- Annual acute care and rehab costs = $9-10 billion
(NIH consensus development panel on rehabilitation 1999) - Estimated annual costs of survivors in 2000 = $60 billion (Finkelstein 2006)
Describe the aetiology of TBI
- Leading cause – RTC (Approx 25-30%)
- Falls - 30-35% (elderly)
- Assaults – 9-10%
- Sports and recreational – 10-20%
- In USA – firearms (10%
What are contusions?
- Bruising of the brain
- Close to bony prominences
- Inferior frontal and temporal poles
Describe diffuse axonal injury (DAI)
- Severe rotation or deceleration force
- Often RTC
- Often loss of consciousness or prolonged low awareness
- Little haemorrhage
- Upon impact the neuron is stretched and compressed
- Cell death may be delayed and not evident for up to 72 hours post injury
- Only 20% seen on CT
- Better seen on MRI
- More widespread damage
What are the types of intracranial bleeds?
- Extradural haematomas - Most dangerous but good recovery if drained
- Subdural haematomas
- Subarachnoid bleed
- Intracerebral/intraventricular bleed
- Basal skull fractures – infection, CSF leaks
What are the two mechanisms of injury in TBI?
Primary and Secondary
Describe primary injuries in TBI
injury at the moment of impact or immediately afterwards o Contusions, bleeding, skull fracture o Coup/contrecoup o Stretch and shearing of neurons o Limited scope for change
Describe secondary injuries in TBI
further injury caused by subsequent events including poor care
o Altered cerebral blood flow – autoregulation
o Hypotension – relation to ICP and CPP
o Release of neurotoxic compounds
Cellular inflammatory response
Cytokines
Calcium influx
Oxygen free radicals
o One episode of hypotension can increase mortality by 50%
o Hypoxia, hypotension, free radicals/cytokines/EAA, cerebral oedema, increase ICP, infection, hydrocephalus, herniation
When should a CT scan be performed within one hour of presentation with a TBI?
- GCS <13 when first assessed or GCS <15 2 hours after injury
- Suspected open or depressed skull fracture
- Signs of base of skill fracture
- Post-traumatic seizure
- Focal neurological deficit
- > 1 episode of vomiting
Describe the immediate management of TBI
- ABCDE
- Oxygenate/intubate
- IV Fluids
- Glucose
- Seizures – diazepam PR/IV, consider prophylaxis
- Drug or alcohol intoxication?
- Electrolytes and acid base status
- Sedation
- Analgesia
- Consult neurosurgeons/orthopaedics
- CT scan once stable
- Surgical treatment (<2%)
- Treat ICP if suspected
- Steroids have shown no benefits in acute TBI
- Seizure prophylaxis beyond 1 week
- Antibiotics or vaccine prophylaxis?
What should be given in the case of drug or alcohol intoxication? (Specifically to each drug)
o Opioids – naloxone o Alcohol – thiamine o Tricyclics (anticholinergics) – physostigmine o Benzodiazepines – flumazenil Also do a toxic profile
How do you treat ICP?
o Mannitol/hypertonic saline
o CSF drain
o Tilt head by 30-40 degrees (better blood flow)
Describe the classification of head injuries
Mild
- GCS 13-15
- Coma <30mins
- PTA <1hr
Moderate
- GCS 9-12
- Coma 30mins-6hrs
- PTA 1-24hrs
Severe
- GCS <9
- Coma >6hrs
- PTA >1day
Name some neurological sequelae of brain injury
- Cranial nerves
o Anosmia, vision, diplopia/strabismus, hearing and balance - Motor
o Paralysis (mono-, hemi-, quadriplegia), ataxia, dyspraxia, tremor, spasticity - Sensory
o Anaesthesia, pain syndromes - Autonomic
o Bladder, bowels, cardiovascular, respiratory, gut, sexual function - Spinal cord injury
- Peripheral nerve injury
- Epilepsy
Name some cognitive changes after brain injury
- Memory
- Attention
- Communication
- Speed of processing
- Visuospatial
- Problem solving/planning
- Mood/anxiety
- Fatigue
- Judgement
- Emotional/behavioural control
- Initiation of actions
Very briefly describe the evidence for early rehab following a brain injury
- Strong (Grade A) evidence that intensive rehab leads to earlier functional gains
o (Cochrane, RCT 351 studies) - Strong (Grade A) evidence that early rehabilitation leads to reduced length of stay in hospital and improved outcomes
o (NSF Typology, Non-RCT 1905 studies)
Describe post-acute rehab following a brain injury
- Primarily addresses regaining mobility and independence in self-care to allow the individual to manage safely at home
- Interventions focus on improving ability and independence (reducing disability)
- In-patient pathways to reduce variation
What are the ABCs of rehab?
Anticoagulation
o Medical
o Ted stockings
o Flowtron
Bladder/bowl
Chest complications
o PE
o Tubes
o Infections
(Neuro)disability assessment
Electrolytes and fluid
Feeding – NG, PEG
Describe medium to longer term rehab of brain injury
- Best provided in the community
- Functional gains to achieve independent living
- Vocational rehab – return to work or alternative employment
- Addressing emotional and psychological issues
- Importance of individual wishes
What are some long term issues following a brain injury?
- Employment
- Dependents
- Psychological support (family)
- Cognitive sequelae
- Behaviours including alcohol
- Driving
- Sex
- Exercise
Name some post head injury symptoms
Poor concentration (most common) Irritability Tired a lot Depression Memory problems Headaches Anxiety Trouble thinking Dizziness Blurry or double vision Sensitivity to bright light
What can post head injury symptoms be assessed by?
The Rivermead post-concussion score
What is post-concussion syndrome?
set of symptoms that may continue for weeks, months, or a year or more after a concussion – a mild form of traumatic brain injury
- 25% of mild TBIs at 3 months, 10% at 1 year (King 2003)
- Physical symptoms decline, psychological increase
What is the double insult theory?
mechanical trauma to the limbic circuits with a maladaptive response
What are the risk factors for post-concussion syndrome?
o Previous brain injury o Female? o Educational level o Past psychiatric history o Genetics? APOE4
What are the perpetuating factors for post-concussion syndrome?
o Alcohol o Other drugs o Depression/Anxiety o Lack of support o Secondary gain – litigation
Name some outcome measures for TBI
- Glasgow outcome scale
- FIM/FAM, Barthel
- Disability rating scale
- Handicap (participation restriction) – Rivermead HI FU questionnaire
- Symptom measures – Rivermead post-concussion score
- BIRCO-39
- QoL measures
Describe the extended glasgow outcome scale
Death
- Dead
Vegetative state
- Unable to obey commands
Lower severe disability
- Dependent on others for care
Upper severe disability
- Independent at home
Lower moderate disability
- Independent at home and outside the home but some physical or mental disability
Upper moderate disability
- Independent at home and outside the home but with some physical or mental disability, with less disruption than LMD
Lower good recovery
- Able to resume normal activities with some injury related problems
Upper good recovery
- No injury related problems
Name factors that can affect prognosis pre-injury
- Age
o Increased mortality in elderly (>65 yrs) and children below 5 yrs - Female, ethnicity, education
- Recurrent head trauma
o Additive damage - Substance abuse
o Increased acute complications, mortality, longer hospitalisations, worse discharge status - Psychosocial factors
o Psychiatric illness/personality
o Lack of family/social support
Name factors about the injury that can affect prognosis
- Aetiology
- Severity of injury
- Care/resus delay (secondary injury extent)
- Unilateral/bilateral
- Scan findings
- Associated injuries
Name factors that can affect prognosis post injury
- Medical care
o Delay in care or transportation increases the chances of secondary complications
o Hypotension and hypoxia are avoidable complications - Complications
o Pulmonary, cardiovascular, haematological or infectious problems associated with poor outcomes - Rehabilitation – both inpatient and community
- Family support
- Health behaviours e.g. substance abuse
- Work – does it protect?
How are TBI patients’ health and life affected?
- Life expectancy
o At least 10 years reduction for severe (McMillan 2013) - People with TBI generally have a propensity towards poor health habits
o Alcohol, smoking, substance use, diet, exercise - At risk for secondary complications (including social e.g. poverty, arrests)
Describe the SHEFBIT cohort study
- From 2012 onwards
- 1322 cases, 1191 at one year
- Shows the affect of TBI on patients lives
- Less than half of patients returned to full work a year after the injury
At 10 weeks
o 39.4% no work, 31.7% less work, 28.9% same
o 55% depression, 61% anxiety on HOADS
o High scores on Rivermead questionnaires
At 1 year
o 23.8% no work, 27.5% less work, 43.9% same
o Depression 41%, anxiety 43%
o Still high scores in Rivermead questionnaires
Describe seizure timing post TBI
- Immediate seizures – occur <24hrs after injury
- Early seizures – occur <1 week after injury
- Late seizures – occur >1 week after injury and constitute the diagnosis of post traumatic epilepsy
- Concussive seizures – immediately after and not epilepsy – no increased risk
What are the risk factors of post traumatic epilepsy?
Systematic review and meta-analysis (Xu et al, 2017)
o Male o History of alcohol abuse o Post traumatic amnesia o Focal neurological signs o Loss of consciousness o Skull fracture o Midline shift o Brain confusion o Subdural haemorrhage o Intracerebral haemorrhage o Mild brain injury o Severe brain injury o Acute symptomatic seizure
- Also found that the aetiology of TBI (fall accident, traffic accident, others) and initial GCS were not a risk factor nor was the presence of a subarachnoid haemorrhage
Describe the risk of seizure following TBI
Population based study published in 1998 (Annegers et al) looked at the probably of seizures after severe, moderate and mild brain injury
o All injuries increased risk of epilepsy over 30 years post injury
o Severe injury was markedly higher than the other two (15% risk over 30 years)
o Mild injury almost the same as baseline
A further study published in Lancet in 2009 (Christensen et al) also looked at the long-term risk of epilepsy after traumatic brain injury
o Split into mild brain injury, severe brain injury and skull fracture
o Found that all groups increased risk
o Most increased with severe brain injury less than a year after injury then decreased as years after injury increased
Describe the relationship between temporal lobe injury and PTE
- Longitudinal study by Tubi et al argues that early seizures and temporal lobe trauma predict PTE
- 90 patients with moderate to severe TBI – 26.7% patients had acute symptomatic seizures, of which 75% had haemorrhagic temporal lobe injury on admission
- 46 patients entered long term follow up, of which 45.7% developed PTE within 2 years
o 85.6% had haemorrhagic temporal lobe injury on admission (compared to 30.6% who did not develop PTE)
o 38.1% had seizures on continuous EEG during acute ICU stay
What is the risk of an early seizure following a TBI?
The risk of early seizures ranges from abut 2% (Temkin et al, 1990; Annegers et al, 1998) in population-based studies to 14-30% in patients with severe TBI (Temkin et al, 1990)
Describe the epileptogenesis theory following TBI
- Latent period between injury and development of PTE
- Proposed latent period events leading to PTE
Initial structural injury o Focal (contusions, haemorrhage, penetrating injury) o Diffuse – diffuse axonal injury
Secondary injury Excitotoxicity o Apoptosis o Neuroinflammation o Oxidative stress
Spontaneous seizures
o Neuronal loss, and neurogenesis – network reorganisation
o Hippocampal sclerosis
o Chronic neuroinflammation
What are the risk factors for early seizures following a TBI?
Risk factors for early seizure have been reviewed by Temkin (2003), who reported that depressed skull fracture, intracerebral hematoma, and subdural hematoma were associated with about a 25% risk of immediate or early posttraumatic seizures
What are the significance of immediate and early seizures following a TBI?
Immediate seizures and early seizures are risk factors for the development of later epilepsy (Temkin, 2003) and seizures within the first 24 hours have been used to identify patients with a high risk of epilepsy after TBI to select for studies of prevention of PTE (Temkin et al, 1990)
Name the non-pharmacological treatment options of epilepsy
- Vagal nerve stimulation (VNS)
- Deep brain stimulation (DBS)
- Resective surgery/Gamma knife surgery
- Dietary approaches
What is VNS?
- VNS is suitable for seizures with a focal or generalised onset
- Involves implantation of a stimulator (pulse generator) into a pocket of skin, under the collar bone or close to the armpit
- Wires, with electrodes, are connected inside the body to the left of the Vagus nerve -The electrodes encase the Vagus nerve in the neck
- Aims to reduce seizure activity by interrupting and preventing the electrical irregularities on the surface of the brain that cause seizures
What are some additional benefits of VNS?
o Improved alertness
o Improved memory
o Fewer mood problems
What are some disadvantages of VNS?
- Not beneficial across the whole spectrum of patients
- Not possible to know in advance who will have seizure reduction
- Can take anything from several months to 2yrs to achieve optimal seizure control
- Mild side effects
What is DBS?
- For patients with seizures of focal onset
- May be appropriate for people unsuitable for resective surgery
- Involves implanting electrodes into specific areas of the brain
- Aims to control excess electrical activity in the rain using regular electrical impulses to reduce the frequency and severity of seizures
o During DBS, a thin wire is implanted into the brain which is connected to an electrical stimulator, which is placed under the skin of the chest - Trials show that for some people their seizures become much less frequent while others it has little to no effect (Epilepsy society 2012)
- DBS stimulation results in reduced seizure frequency of 69% (medtronic 2015)
What are some disadvantages of DBS?
- Almost the same as for VNS
- Not widely available in the UK at present – only available in Sheffield for dystonia and PD
- The evidence on the efficacy of DBS for refractory epilepsy is limited in both quantity and quality
o The evidence on safety shows that there are serious but well-known side effects
o Should only be used with special arrangements for clinical governance, consent, and audit or research
o (NICE Jan 2012)
Describe epilepsy surgeries
- May be suitable for patients with focal onset seizures
- If several AEDs trialled and none of them have stopped or significantly reduced seizure frequency (50%)
- If a psychical cause for epilepsy, such as scarring on the brain or damage to the brain from a head injury, or following an infection such as meningitis, can be identified on scans and is only in one area of the brain
- Around 70% of people become seizure free (Epilepsy society 2013)
- Surgical intervention = resective and/or disconnected procedure
Describe resective procedures for epilepsy
o Different types of lobectomy (e.g. temporal, frontal etc)
o Topectomy – excision of a small area tailored to the seizure focus itself
o Hemispherectomy – the ultimate focal resection with the removal of one half of the brain
o More likely to result in a cure since they excise
Describe disconnective procedures for epilepsy
o Corpus callosotomy
o Multiple pial transections
o Tend to more palliative rather than curative as they interrupt the propagation of the seizures, limiting their generalisation
What are the disadvantages of epilepsy surgery?
- Carries significant risks – death, stroke, paralysis, worsening of epilepsy
- Implications for people previously requiring carers, becoming independent and losing their epilepsy
- Approx 50% of patients recommended are unable to proceed after formal testing
What is gamma knife surgery?
- Narrow beams of radiation targeted to precisely defined volume of tissue within the brain
- Highly focused and destructive dose of radiation is given in a single session and avoids potentially harmful radiation to surrounding brain structures
- Often a safer option than traditional brain surgery
- Total treatment time varies from 45 to 90 minutes
What are some side effects of gamma knife surgery?
Almost no initial effects of radiosurgery
o Local pain to the scalp, responds to simple, oral pain medication
Long range effects after many months
o Swelling within the adjacent brain which may cause symptoms such as headache and neurological disturbances
o Treat with oral steroids and is self-limiting
Permanent cranial nerve dysfunction is rare with modern gamma ray doses
What are the benefits of gamma knife surgery?
- Non-invasive
- No incision, no need for head shaving, no scars to heal
- No hair loss or nausea
- Treatment is relatively painless and in most cases a GA is not needed
- Patients make a fast recovery and can usually resume their normal activities in a day or two
What are ketogenic diet therapies?
- Range of high-fat and low carbohydrate diets which mimic the metabolic effects of prolonged fasting
- One treatment option for children whose seizures are not controlled with AEDs
- Ketones are formed when the body uses fat for its source of energy
- Because the ketogenic diet is very low in carbohydrates, fats become the primary fuel instead
- Higher ketone levels often lead to more improved seizure control
- Particularly recommended for children with Lennox-Gastaut syndrome
- Not usually recommended for adults as the diet is very restrictive
Can a ketogenic diet ever be stopped?
- If seizures have been well controlled for some time, usually 2 years, it might be suggested to go off the diet
- Patient is gradually taken off over several months – seizures may worsen if the ketogenic diet is suddenly stopped
- Children usually continue to take AEDs after stopping the diet
What are the potential side effects of a ketogenic diet?
- Kidney stones
- High cholesterol levels in the blood
- Dehydration
- Constipation
- Slowed growth or weight gain
- Bone fractures
What are some potential triggers of photosensitive epilepsy?
o Faulty florescent light strips that flicker
o Christmas tree lights (except those put up by public organisations)
o Flashing novelty badges
o Red flashing bicycle lights (when very close)
o Light seen through a fast-rotating ceiling fan
o Some films with flashing or flickering images
o Strobe lighting (night clubs, theme parks) – in the UK this is restricted
o Older TV screens – use LCD screen
What are some ways of avoiding a photosensitive seizure?
o Consider covering one eye – reduces the number of brain cells that are stimulated
o Any dizziness, blurred vision, loss of awareness or muscle twitching – stop looking at the screen immediately
o Take frequent rests
What are the psychological associations of epilepsy?
- Co-morbid depression/anxiety – those with refractory epilepsy at high risk
- Low self-esteem
- Psychosocial problems
o Education
o Employment
o Relationships
o Social isolation - Psychosis
- Self-harm
- Anger issues and violence
- Adjustment/acceptance issues
- Suicidal thoughts, attempts and actual suicide
- Sleep disturbance
(Dewhurst 2010)
What is the psychological management of epilepsy
- Currently limited evidence for the effectiveness of interventions to improve the health and quality of life in people with epilepsy
- Specialist nurse and self-management education have some evidence of benefit
- At present it is not possible to advocate any single model of service provision
(Cochrane review 2016)
What is status epilepticus?
Maximum expression of epilepsy
Seizure that last longer than 5 mins or multiple seizures without recovery
o Most seizures last less than 5 minutes
o Those that last longer do no stop spontaneously
o Seizures become self-sustaining with neuronal injury within 15-30 mins
What are the types of status epilepticus?
- Generalised status epilepticus
- Complex partial status epilepticus
- Epilepsia partialis continua
Describe the epidemiology of status epilepticus
- Incidence 10-41/100,000
- Lifetime risk 10% in patients with epilepsy
- Mortality 9-60%
- Severe neurological/cognitive morbidity – 11-16%
- Status longer than 30mins = 20% mortality
Describe convulsive status epilepticus
- Convulsions associated with rhythmic jerking
- Generalised tonic-clonic movements
- Mental status impairment
- Focal neurological deficit
Describe non-convulsive status epilepticus
Seizures activity on EEG without clinical findings of GCSE
o Wandering confused, automatisms
o Acutely ill, obtunded (less than full awareness) ± motor abnormalities
Negative symptoms
o Anorexia, aphasia/mutism, amnesia, catatonia, coma, confusion, lethargy, and staring
Positive symptoms
o Agitation/aggression
o Automatisms, blinking, facial twitching
o Delusions, echolalia, laughter, nausea/vomiting
o Nystagmus/eye deviation
o Psychosis
Describe the process of seizure to status
Minutes
- Receptors move from synaptic membranes and endosomes
- GABAergic receptors destroyed – less responsive to neurotransmitter/GABAergic drugs
o Metabolic changes within cells
o Potency of benzodiazepines reduces by 20-fold after 30 minutes (GABAergic)
- NMDA and AMPA (glutamate) receptors move to the synaptic membrane causing further excitation
Minutes to hours
- Increased proconvulsive neuropeptides depletion of inhibitor neuropeptides – increased excitability
Hours to weeks
- Long term gene expression changes as result of neuronal death and reorganisation
- Seizures inhibit brain synthesis
What is the aetiology of status epilepticus?
- Low levels of AED in epilepsy (34%)
- Remote brain injury/congenital malformation (24%) - >1 week after an insult that could cause epilepsy
- Cerebrovascular accident (22%)
- Drug/alcohol withdrawal (10%)
- Brain infections/inflammation (5%)
- Metabolic problems e.g. low sodium (15%)
What problems arise from an ongoing seizure?
Sympathetic overdrive o Increased cardiac output o Increased blood pressure o Increased blood sugar o Increased blood lactate
Decompensation o Cardiorespiratory collapse o Electrolyte imbalance o Rhabdomyolysis (muscle breakdown) – acute tubular necrosis (kidney failure) o Hyperthermia o Major organ failure o Cerebral oedema
What is the management in the 1st stage of SE (0-10mins)?
- ABCDEFG
- Secure airway
- High flow oxygen
- Cardiac and respiratory function
- Obtain IV access in a large vein
- Check blood glucose levels
What is the management in the 2nd stage of SE (0-30mins)?
- Regular monitoring
- Consider the possibility of NEAD/pregnancy
- Emergency AED therapy
- Emergency investigations (bloods, arterial gasses)
- Consider glucose (dextrose) ± high dose IV pabrinex (vitamin B and C) if low nutrition
- Treat severe acidosis
What is the management in the 3rd stage of SE (0-60mins) - established status?
Seizures that resolve quickly suggest something is fuelling them
o What is the cause?
o Is there something else maintaining them?
o Are we giving the right treatment?
Prolonged seizures are dangerous
o Airway: obstruction, secretions, aspiration
o Breathing: hypoxia
o Cardiovascular instability: hypotension, cardiac arrhythmias
o Disability: neurological problems and risk of injury
What is the management in the 4th stage of SE (30-90mins) - refractory status?
- ICU
- Anaesthesia advantages
o Powerful AED effects
o Can protect the airways
o Can get scans and treat easily
- Anaesthesia disadvantages o Pneumonia o Hypotension and cardiac arrhythmias o Not moving is bad – poorer outcomes o Infection
- Give more AED?
o 70% get inadequate loading dose of first AED
What are some consequences of coma/ICU as a result of SE?
- Immobility o Pressure sores o DVT o Pneumonia o Muscle weakness
- Organ dysfunction
o GI tract
o Immune system (including hospital acquired infections) - Psychological impacts (PTSD)
Why does the patient stopping moving not necessarily mean the seizure has stopped in SE?
o Usually anaesthesia induction requires a paralysing drug
o Often paralysis is needed for the ventilation of the patient
o After a long seizure movement diminishes
How can you determine a seizure has actually ceased in SE?
Use EEG
o Can see ongoing seizure activity
o Can suggest other causes e.g. Encephalitis, NEAD
What is the first line drug in SE?
Benzodiazepines (e.g. Lorazepam, diazepam, midazolam)
o Gaba receptor targets
o Slow all neurotransmission including consciousness and breathing
o Can last a while and can hide and accumulate
o Take some time to work
o Can be given IV, PR, buccal, IM, orally
o Grade A/B evidence – they work
What is the second line drug is SE?
- Phenytoin (Ideally fosphenytoin)
o Works well – grade B evidence
o Risks including cardiac problems
What drugs should be given third line and beyond in SE?
o Evidence is limited
o Phenobarbitone, levetiracetam, valproate
o Anaesthesia – thiopentone, propofol
Describe the ongoing management of SE
- Review/continue regular AEDs - Risk of recurrent seizures after status 41%
- Get drug history
- Drug levels
- NG feed and drugs
- Consider NEAD/maintaining factors
- Consider out of hospital management of seizures
- Consider compliance
How is refractory status defined?
Seizures that continue despite two
o Appropriate AEDs at
o Appropriate does
Duration not relevant – can go on for months
What is the mortality of refractory status?
23-60%
What are some predictors of refractory and non-refractory status?
Refractory
- Encephalitis
- Hyponatraemia
- Longer duration
- More seizure activity
- Poor outcomes if Epilepsy or NICU stay
Non-refractory
- Low AED levels
- 44% admitted to ICU received inadequate prior doses
Name some other strategies that could be considered for refractory status
o Valproate – risk of encephalopathy o Keppra o Topiramate (via NG tube) o Ketamine o Steroids – if any suspicion of autoimmune encephalitis o Hypothermia – some case reports o Lidocaine o Paraldehyde o Chlormethiazole o Clonazepam o Lacosamide o Ketogenic diet o Electroconvulsive treatment (case report/series) o Vagus nerve stimulation o Surgery (case report, resect epileptogenic lesion)
What is primary healthcare?
o First point of contact for health care
o For new problems (including urgent and emergency) and for ongoing problems
o Places – GP practices, Walk-in centres, minor injury units, dentists, opticians, ?999, ?A&E
o Wide range of practitioners
o Not the same as general practice
What is expert medical generalism?
- Provision of health care to all patients with any health care need
- Its focus is on the person and not the disease – whole person medicine
Describe the relevance of diversity and breadth knowledgebase in GPs
- The diversity and breadth of the GP knowledgebase it its essence
- GPs have depth of knowledge in lots of high prevalence diseases
o Asthma, COPD, diabetes, hypertension, headache - But they do not have deep knowledge of all conditions especially rare conditions
- Therefore – GP requires decision making often without subject specific expertise
What clinical skills and clinical reasoning do GPs require?
- History and examination are the essential foundations of good clinical judgement
- Need to be able to rapidly take a focused clinical history
o GP appointments are only 10 mins long - Need to understand the principles of epidemiology – incidence and prevalence
- Pragmatic and rapid clinical examination of all body systems
- Make clinical decisions and risk management an issue of shared decision making
- Based on trust and longitudinal relationships
What is the quality outcome framework (QOF)?
- Part of the GP contract since 2004
- Sets targets (indicators) for clinical outcomes
- Meeting targets is associated with additional income
- This income reflects the resources required to achieve these targets
- Conditions include
o Atrial fibrillation
o Secondary prevention of coronary heart disease
o Hypertension
o Diabetes
o Dementia
o Depression
o Cancer
o Epilepsy
o Cardiovascular disease
o Blood pressure
o Obesity
o Smoking - Important for neurological disease
What is the issue of multi-morbidity and evidence based medicine?
- Most of evidence-based medicine is based on a single disease model
- But increasingly patients have more than one long-term condition
- Technical and practical challenges of managing multi-morbidity
o How to manage inconsistencies between guidelines?
Describe general practice within the NHS
- General practice is the largest medical/surgical speciality
- 34,242 FTE GPs in England
- Working in 7,500 practices
- Average list size – 6,610-7,171
- Patients per GP – 1,577
- Estimated 372 million GP consultations each year
- 90% of all NHS patient contacts occur in general practice
- Average member of public sees GP six times per year
- GPs make most diagnoses in the NH - Therefore, most neurological diagnoses
- 8.39% of NHS funding
- Comprehensive primary care lowers the overall cost of healthcare systems
- £136 per patient per year for unlimited general practice care - About the same as the cost of a single visit to a hospital outpatient department
What is primary care neurology?
- GPs as expert medical generalists
- Working in extended teams to diagnose and manage neurological illness
- Not a disease-based model but a person-centred model
- Providing tailored personalised care
- Characterised by on-demand access, continuity and individual relationships
- Diagnosis and treatment of disease
- But also, prevention of disease and promotion of health
- Basing most practice on clinical skills (not investigations)
- Clinically effective and cost-effective care
Define stroke
an acute onset of focal neurology (or global neurological dysfunction) leading to death, or lasting longer than 24 hours as a result of damage to the CNS that is vascular in origin
Define TIA
lasts less than 24 hours by definition but generally less than 1 hour
Describe the impact of stroke
- 15 million people/year worldwide suffer a stroke
- In UK, approximately 152,000 people have a stroke every year
- 4th leading cause of death in UK and major cause of adult disability
- Lifetime risk of suffering a stroke in men is 1 in 4 while it is 1 in 5 in women
- Majority over the age of 65 but 25% occur in under 65
Name some modifiable risk factors for stroke
o Hypertension o AF – increases risk by 7-8 times (anticoagulation reduces excess risk by 90%) o High cholesterol o Vascular disease o Diabetes and metabolic syndrome o Heart failure o Smoking/drug use/alcohol abuse o Physical inactivity/obesity/diet o Contraceptive pills o Thrombophilia o Hyperhomocysteinaemia o Obstructive sleep apnoea
Name some non-modifiable risk factors for stroke
o Age o Gender o Ethnicity o Genetic predisposition o Previous TIA/stroke
Describe cerebral perfusion and its relation to brain health
- CBF – 50ml/100g/min
- About 20% of CO
- Can compensate until CBF reduced to 20-25ml/100g/min
- CBF relatively constant when mean arterial blood pressures are between 50-150mmHg
- If CBF <10ml/100g/min all membranes and functions severely affected
- Neurons cannot live long at <5ml/100g/min
What symptoms would indicate a frontal lobe lesion?
- Disinhibition
- Apathy
- Irritability
- Inappropriate placidity
- Obsessional behaviour
- Distractibility
- Poor planning skills
- Utilisation behaviour
- Release of primitive reflexes (e.g. pout)
- Gait apraxia
Name the two types of stroke
- Ischaemic (85%)
- Haemorrhagic (15%)
What are the aetiologies of ischaemic stroke?
- Carotid disease and vertebrobasilar disease
- Carotid stenosis – chronic atherosclerosis disease
- Plaque rupture with either thrombosis (causing stenosis/occlusion) or embolism
- Dissection – usually history of trauma with neck pain and can be associated with Horner’s syndrome
- Embolic sources
- Prothrombotic states
- Hypoperfusion
Name some embolic sources of stroke
o AF
o Paradoxical emboli and PFO (patent foramen ovale)
o SBE (subacute bacterial endocarditis)
o LV thrombus/post MI
o Mechanical valves (usually with suboptimal anticoagulation)
o Post-operative carotid/peripheral vascular/valvular/cardiac surgery
Name some prothrombotic states
o Antiphospholipid syndrome
o Polycythaemia and hyperviscosity syndrome
o Malignancy
Name some causes of hypoperfusion
o All causes e.g. sepsis, iatrogenic, hypovolaemia
o Must look for carotid stenosis – generally hypotension must have been prolonged and severe to cause stroke
o Also – inflammatory causes such as vasculitis
What are some aetiologies of haemorrhage stroke?
Rupture of vessels
o Through excessive pressure (hypertension) o Or friable/damaged vessels Vasculitis Amyloid angiopathy Vascular malformations Moyamoya o Trauma e.g. traumatic SAH o Malignancy
What is the presentation of an anterior circulation stroke?
o Hemiplegia o Hemisensory loss o Neglect/inattention o Speech problems o Amaurosis fugax
What is the presentation of a posterior circulation stroke?
o Balance problems o Visual field defects o Swallowing problems o Poor coordination o Drowsiness o Cognitive issues (thalamic involvement)
What is the presentation of haemorrhagic stroke?
Can be any of anterior and posterior circulation defects
More commonly associated with headache
Drowsiness can be prominent especially in a large bleed
Describe the pattern of motor weakness following a stroke
o Hemiparesis
o Focal single limb/facial weakness, could be proximal or distal
o Pyramidal in pattern
o Initially reflexes are down but as spasticity develops will become more pronounced
o Plantar reflexes
o Palatal weakness – dysphagia, dysarthria
o Unilateral
What is an example of a peripheral nerve distribution of weakness and therefore not a stroke syndrome?
Bell’s palsy is not a stroke syndrome
Stroke is a UMN lesion and therefore is forehead sparing – facial motor output as projection from both hemispheres
Describe the patterns of sensory loss in a stroke
o Hemisensory loss o Confined to one limb o Unilateral o Does not cross the midline o Generally multimodal o Look for cortical dysfunction such as stereognosis or graphesthesia
What sensory deficits would suggest it’s not a stroke?
o Positive sensory phenomena generally do not occur in stroke
o Peripheral nerve distribution
o Sensory levels
o Bilateral symptoms
Describe the oxford classification of stroke
Total anterior circulation syndrome (TACS)
o All 3 of unilateral weakness/sensory deficit, homonymous hemianopia, higher cerebral dysfunction (dysphasia, inattention/neglect)
Partial anterior circulation syndrome (PACS)
o Either 2 of the above or higher cerebral dysfunction alone
Posterior circulation stroke syndrome (POCS)
o Any of: ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit, bilateral motor and/or sensory deficit, disorder of conjugate eye movement, cerebellar dysfunction, isolated homonymous visual defect
Lacunar stroke syndrome (LACS)
o Pure hemi-motor, pure hemi-sensory-moor, ataxic hemiparesis
Why are TIAs important for stroke?
- 20% of patients with stroke report a preceding TIA
- Identify and treat if possible high-risk individuals to prevent a subsequent more serious event
What is the ABCD2 score and what is it used for?
o Use for triaging high risk patients
o Target rapid intervene to high risk patients
o Age, Blood pressure, clinical symptoms, duration of symptoms, diabetes
What is deemed a high risk TIA?
- AF
- Known carotid stenosis
- Crescendo TIAs
- On anticoagulation
- Give specialist review within 24 hours
What is large vessel disease?
- Atherosclerosis of large and medium sized arteries
Describe the mechanisms for large vessel disease
o Thrombus on lesion causing local occlusion
o Embolisation of plaque debris or thrombus in distal vessel
o Small vessel origin occlusion by growth of plaque
o Severe reduction in diameter of vessel lumen leads to hypoperfusion and infarction of distal watershed areas
Describe small vessel disease
- Small penetrating arteries of the brain
- Occlusion of these causes infarction – Lacunar
- Small vessel arteriopathy – hyaline arteriosclerosis
o Muscle and elastic in arterial wall replaced by collagen
o Wall thickening with subsequent lumen narrowing - Diabetes, hypertension, age
What are some causes of cardioembolism?
- Atrial fibrillation (LA thrombus) – 80%
- Myocardial infarction (anterior wall) with hypokinetic wall segment/LV aneurysm
- Infective endocarditis
- Non-bacterial thrombotic endocarditis
- Prosthetic heart valves (mitral)
- Paradoxical embolus – PFO, ASD, VSD
What is the importance of AF in stroke?
- Overall 5x increased risk of stroke
- Around 25% of people over 80 having AF
- AF strokes 3x more likely to be classed severe
o Clots can form in the left atrial appendage
o Can become large before embolising
o Fibrin rich clots
Name some obscure causes of stroke
- Arterial dissection and trauma
- Inflammatory vascular disease
o GCA, SLE, antiphospholipid syndrome, RhA - Haematological
o Thrombophilia, leukaemia, lymphoma, polycythaemia, sick cell, TTP, DIC - Peri-operative
o Anaesthetic – reduces CO, can precipitate irregular heart rhythm - Recreational drugs
o Cocaine, amphetamines
What can cause primary intracerebral haemorrhage?
- Intracranial small vessel disease – HTN
- Cerebral amyloid angiography
- AMVs
- CNS neoplasms
- Anticoagulation
What is the estimated cost of stroke in the UK?
At least £7 billion every year
Describe blood pressure and its effect on stroke risk
- High = BP> 140/90
- In most countries >30% adults suffer from high blood pressure
- Most important modifiable risk factor for stroke
- For every 10 deaths from stroke, 4 preventable if BP treated
- Blood pressure linked to BMI, physical activity and dietary salt intake
- BP tends to increase with age except where obesity is absent, salt intake low and physical exercise high
What is the population-based approach to stroke prevention?
Education regarding healthy lifestyle including
o Increased exercise
o Lower salt intake
o Better diet – more fruit and vegetables
o Reduced cholesterol intake
o Reduced alcohol intake
o Stop smoking
Describe smoking and stroke
- Doubles the risk of stroke in men and women
- Several mechanisms involved – damages endothelial lining, promotes atheroma, enhances clotting, raises LDL, lowers HDL, raised BP
- Stopping smoking reduces cardiovascular risk to close of that of a non-smoker
Describe cholesterol and stroke
- High total cholesterol, high LDL and low HDL are important risk factors for IHD
- Causal association for stroke not so clear
- Pooled data suggests high levels of cholesterol risk factor for ischaemic stroke but not ICH
- Clear evidence from trials of benefit of lowering cholesterol in patients with history of IHD, PVD or prior stroke on preventing further events
Describe the treatment of high cholesterol
Statins!
o Reduce cholesterol and have effects on platelets and vascular endothelium
o Reduces the risk of MI, of stroke and of revascularisation by at least one third
o 5 years of statins prevents major vascular events in about 70 out of 1000 with previous stroke (Heart protection study 2001)
Describe social deprivation and its effect on stroke risk
- People living in deprived areas are 3 times more likely to die from stroke than the least deprived
- Been attributed to higher rates of smoking, poor diet, obesity, lack of exercise
Describe AF and its effect on stroke risk
- NVAF associated with 6-fold increase in risk of stroke
- Individuals risk is compounded by other risk factors (E.g. CHF, PVD, high BP, elderly, diabetes, female)
- Treatment options include aspirin, warfarin or one of the NAOCs
- CHADS2VASC score predicts risk of stroke
- HASBLED score predicts individual risk of haemorrhage on treatment
Describe the primary prevention of stroke
Targeting at risk groups
- Identify high risk population
- Regular BP checks
- Well man clinics
- Diabetes/high cholesterol/AF
- Assess overall cardiovascular risk prior to treatment
Describe some secondary prevention strategies for stroke
- Rapid assessment of patients with TIA
- Address cardiovascular risk factors
- BP <130/80, <120/80 in diabetes
- Statin for all patients
- Antiplatelet – reduces risk by around 20% annually
o Clopidogrel or aspirin and dipyridamole combination - Warfarin/DOACs for patients with AF
- Carotid endarterectomy for patients with tight symptomatic stenosis
Name the two types of haemorrhagic stroke
- Subarachnoid haemorrhage – occurs when a blood vessel on the brain surface ruptures (aneurysm/AVM)
- Intracerebral haemorrhage – occurs when a blood vessel bleeds into the tissue deep within the brain
Describe intracerebral haemorrhage and its epidemiology
- 10% of strokes
- Within bran parenchyma
- 12-15/100,000 per year
- Incidence >55yrs increases and x2 with each decade until >80yrs then x25
- Previous CVA risk increases risk x23
- Onset usually during activity
What is the most common site of an intracerebral haemorrhage?
Basal ganglia/ Putamen/ Lentiform Nucleus/ Internal capsule/ Globus pallidus in 50%
Name some common arterial feeders
- Lenticulostriates – sources of Putaminal haemorrhages
o Possibly secondary to microaneurysms of Charcot Bouchard (caused by chronic hypertension) - Thalamoperforators – supplies thalamus
- Paramedian branches of Basilar artery
What can cause increased CBF? (and therefore haemorrhagic stroke)
o Haemorrhagic transformation – type 1 and 2 (post ischaemic stroke)
o Migraine
o Exercise
o Cold
Name some vascular anomalies
o AVM o Aneurysm o Cavernoma o Amyloid angiopathy o Cerebral venous thrombosis
What types of tumours can cause a hemorrhagic stroke?
Metastatic malignant melanoma, renal, thyroid and lung carcinoma, choriocarcinoma, Oligodendroma ependymoma
Describe the presentation of haemorrhagic stroke
Putaminal
o Most common type – especially in hypertensive haemorrhage
o Contralateral hemiparesis or hemiplegia
Thalamic
o Motor and sensory loss
o Presentation depends on what part of the thalamus is affected
Delayed deterioration can occur
o Rebleeding, oedema, hydrocephalus, seizures
What investigation should be performed if a haemorrhagic stroke is suspected?
- CT is sensitive diagnostically
- MRI may help to differentiate between hypertensive haemorrhage from other causes
Briefly describe the management of haemorrhagic stroke
Standard medical support
o Stop antiplatelet drugs, reverse anticoagulation
Surgical evacuation depends on location, age and premorbid performance status of patient
