Transcript Head Injury - Cambridgecourse.com

Head Injury
Neuropsychiatric aspects
Cambridge MRCPsych Course 2011
Dr Shahid H Zaman
Consultant Psychiatrist , CPFT & Visiting Hon. Fellow, University of Cambridge
[email protected]
Aim
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Understanding of the basics of Head Injury
Pathology
Long-term disabilty
Behavioural & psychiatric aspects
How to recognise (diagnose) and manage
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Post-traumatic seizures
Cognitive impairment
Depression & anxiety
Psychosis
OCD
Emotionalism
Personality disorders
Aggression
Post-concussion syndrome
Principles
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What is “brain injury”?-severity and nature
Bio-psycho-social factors-diagnosis & management
Neuropathology-Diffuse versus focal (open vs. closed)
Acute [what happens immediately after e.g, shunts,
deliruim, min. conscious states etc] versus long-term
consequences
Categories of presentations or symptoms-diagnosis
Seizures
Pre-morbid factors
Interventions
What is a Traumatic Brain Injury?
• “Brain injury caused by trauma to the head
(including the effects upon the brain of other
possible complications of injury, notably
hypoxaemia and hypotension, and
intracerebral haematoma).”
Medical Disability Society (British Society of Rehabilitative Medicine)
• A brain injury can be caused by: trauma, SAH,
CVA, tumours, hypoxia/hypoglycaemia,
encephalitis, meningitis etc
Traumatic Brain Injury
• Injury caused by physical forcesacceleration/deceleration or sheering causing
brain function disruption=“TBI”
• So may have no apparent HI, but have TBI
Closed TBI and Open TBI
• Closed can cause diffuse damage
• Open caused focal injury-penetrate dura
Size of the problem
• 200-300/100,000 attend hospital with HI p.a.
• 1/6 admitted (80% mild, 10% moderate and
10% severe)
• Prevalence of considerable disability as a
result of HI is 100 per 100 000
Demographics & Risk Factors
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High risk: 15 to 25 yr olds
2-3 males to 1 female
Alcohol
Low socioeconomic groups
RTA biggest cause then assaults and falls
(some deliberate self-harm)
In General Adult Psychiatry
• Taking a good history of head trauma
• Be specific
• Ask about vehicle accidents, falls, assaults,
sports injuries, alcohol
• Ask about memory, headaches, concentration,
dizziness, fatigue, irritability, fall in
performance or functioning
• Corroborative evidence
Outcomes
Psychological & psychiatric
symptoms have the biggest impact on
long-term outcomes
Recovery & Rehabilitation
• About what the person can do & not what
cannot
• less focus on categorising “health” from
“disease”-i.e. think of a spectrum
• Greater emphasis on environmental
interventions & an enabling environment
• Quality of life determinants inc. social,
occupational, leisure, hope, spiritual etc.
Function & Dysfunction
• Impairment-anatomy, physiology, psychology
• Disability-impairment that prevents the
performance of activities
• Handicap-disadvantaged condition deriving
from impairment or disability limiting a person
performing a role considered normal in
respect of their age, sex and social and
cultural factors
International Classification of Impairments, Disabilities and Handicaps
Example
TBI
Hemiplegic/spasticity
Wheelchair mobile
impairment
Disability-limits activity
X
handicap
stairs
ramp
Handicap-free
Severe
impairment
Degree of handicap
Mild
impairment
Degree of “unfavourable” environment
Closed HI
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Contusion
Diffuse axonal injuries
Haemorrhages
Hypoxia/Ischaemia
Hypotension
Oedema
ICP
Hydrocephalus
Atrophy
Anderson et al., 2006; 6:342-357
Anderson et al., 2006; 6:342-357
Timeline
1st
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secsmins
• Accelerati
on/decele
ration
• Diffuse
• Arteries &
veins
• Skull bone
2nd
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minshrs
• “ABC”
• Hypoxia
• ischaemia
3rd:
Dayswks
• Haemorrhage
• haematomas
• Compression
• Brain swelling
• ICP
Pathology-1
• Intracerebral Haemorrhage: site of contusion; interface between
grey & white matter (associated with diffuse axonal damage); larger
vessels
• Extra-dural haemorrhage: temporary recovery after HI, then death
• Subdural haemorrhage: can be late presentation following HI;
fluctuating course; alcoholics, elderly
• Vasogenic oedema, brain swelling-raises ICP-compromises
circulation; cerebral herniation
• Ischaemia/hypoxia
• Contusions-forces, translational & sheering & rotational; bony
contours: frontal & temporal; contrecoup contusions
Snell, Clinical Neuroanatomy for Medical Students
Neuroanatomical “hotspots”
• Temporal poles & under-side
• Medial orbito-frontal
medial orbital frontal cortex & temporal lobes (tips & under surface) most vulnerable
Pathology-2
• Diffuse axonal injury: after 24-48 hrs; white matter
tracts;
• Axonal swelling, transneuronal degeneration of
undamaged neurons
• Neuronal death: Necrosis & apoptosis
• Altered expression of transcription factors, apoptotic
proteins; lipases, proteases, endonucleases,
oxidative stress response.
• Degradation of cell membranes & cytoskeletal
proteins, mitochondria dysfunction, free radicals
Pathology-3
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Neurotransmitters disrupted
Inflammation
Altered neuroplasticity
Cerebral connectivity-recovery
Neurochemical disruptions
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Serotonin
Acetyl choline
Noradrenaline (Norepinephrine)
Dopamine
CSF Circulation
Snell, Clinical Neuroanatomy for Medical Students
Cranium
Dura mater [sagittal sinus [arachnoid villi]]
Arachnoid mater
Subarachnoid space
[Archnoid trabeculae; vessels; CSF]
Pia mater
Brain
Cranium
Dura mater [sagittal sinus [arachnoid villi]]
Arachnoid mater
Subarachnoid space
[Archnoid trabeculae; vessels; CSF]
Pia mater
Brain
Pathological determinants
• CSF flow
• VP shunt
• Axons
• White matter tracts
• Neuromodulator pathways (spontaneous behaviour, pleasure)
• Arousal systems
• Subdural
• Extradural
• Intra-cerebral
Medical Co-morbidity
• Alcoholism/Substance misuse-may have had
previous injuries, pre-existing alcoholic
damage
• Subdural
• poor physical & psychological health
• poor social circumstances
• Any medical condition
Severity of Traumatic Brain Injury
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Duration of coma (but confounded by intervention)
Duration of PTA (> 1 month, significant disability)
Depth of unconsciousness - GCS
Neurological evidence of brain injury
POOR OUTCOME RISK factors: previous ABI, older,
alcohol, APOE e4
• POOR indicators: retrograde amnesia, presence of
skull fracture, size of blow to head
Severity of Head Injury
Retrograde amnesia
Post-traumatic amnesia
Time of assessment
Glasgow Coma Scale (Verbal; Eye movement; Movement)
Mild (13 to 15 for <30min & PTA of <24 hours)
Moderate (9 to 12 for <6 hours & PTA of >1, but <14 days)
Severe (3 to 8 for >6 hours & PTA of >2 weeks)
Severity of HI
• Mild: amnesia or LOC <30min, no fracture
• Moderate: bet. 30min & 24hrs, non-depressed
fracture
• Severe: more damage or amnesia or LOC
>24hrs)
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A Case-severe TBI, early management
22 year old
April 2005:
RTA, GCS 4/15
Tempero-parietal & basal frontal contusions, SAH, cerebral
oedema, multiple bony injuries (C4-7; L1,2, ribs), spleen & lungs
July 2005
Bi-frontal decompressive craniotomy for intractable
post-op: hydrocephalus, V-P shunt;
seizures, phenytoin, carbamazepine
Sept 2005
Neurorehabilitation Unit; minimally conscious, botox,
baclofen; feeding PEG; incontinence, mobility, skin,
communication
March 2006
Titanium cranioplasty
ICP;
Issues of psychiatric diagnosis post TBI
• No agreed specific nosology: “secondary to medical
conditions” under diagnostic classifications
• Language difficulties limit exploring mental stateimportance of detailed behavioural observations
• Non-specific e.g. TBI-related apathy, anhedonia, sleep
problems, reduced energy, appetite, concentration.
• No clear causal relationship between time of onset of
symptoms and TBI
• TBI may be precipitant for some conditions in
genetically predisposed e.g. schizophrenia
Early Neuropsychiatric Symptoms
• Delirium then disorientated but alert
• Wondering, aggression, sexual disinhibition
• Affect & Mood: apathetic, perplexed, derealisation,
depersonalisation, anxious, agitated, fearful
• Thoughts: disordered, delusional misidentifications,
reduplicative paramnesia (e.g. visited a duplicate
location), delusional disorientation (e.g. believe still
at work even if in hospital), confabulation, delusional
memory,
• Perceptions: visual hallucinations, déjà-vu, illusions
of familiarity
• Insight: no injury-fabricated, no memory problems
Range of conditions
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Psychosis
Depression & anxiety
Mania
PTSD
Agitation & aggression
Personality disorders
Post concussion syndrome
Cognitive dysfunction (amnesia, dysexecutive
syndrome, perceptual abnormalities, language)
• Post traumatic epilepsy
Post-traumatic epilepsy
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Early seizures are benign & not predictive
EEG not predictive
Prophylactic AED do not prevent late seizures
Risk factors: depressed skull fracture,
penetrating injury (5% vs 30%), intracranial
haemorrhage, severity of injury, early seizures,
h/o alcohol abuse
Post-traumatic epilepsy
• 50% in remission in PTE after open HI after 5
years
• Within 5 yrs post-injury, on AED: 1% (mild),
2%(moderate), 12% (severe)
• After 5 yrs, less likely to due to injury
• Associated with psychiatric morbidity e.g.
depression, psychosis (esp. if temporal lobes)
• AEDs and cognitive SE, e.g. phenytoin,
phenobarbitone; carbamazepine is prefered but
can use e.g. lamotrigine, valproate, levetiracetam
Post-HI psychosis
• Is it “post-TBI” or is there any history of
“idiopathic psychosis”?
• Paranoid delusions, auditory hallucinations
55%
• Incidence of 20%
• RISK factors: early injury; left temporal lobe;
cognitive impairment
Kim et al., J Neuropsych Clin Neurosci 2007; 19:106-127
Post-HI psychosis
• Early: Paranoid psychosis, in those with severe
cog impairment & personality change, also
associated with aggression
• Memory impairment facilitates development
of persecutory ideas
• Later: Schizophrenia-like psychosis, assoc with
severity of TBI
Post-HI depression
• Reduced energy, depressed mood,
worthlessness, suicidal ideation
• Incidence: 15.3-33%; prevalence 18.5-61%
• RISK factors: psychosocial stressors; L ant
hemisphere (depression); R hemisphere
(anxious depression); Lateral vs. medial
lesions; age; lack of work; fear of job loss
Kim et al., J Neuropsych Clin Neurosci 2007; 19:106-127
Post-HI depression
• Overlap of symptoms with those of TBI:
apathy, anhedonia, sleep disturbance, poor
appetite & concentration
• Focus on: guilt, worthlessness
• Can further impair cognition
• Associated with aggression
Post-HI Mania
• Insomnia, impaired judgement, grandiosity,
irritability, pressured speech (80-100%),
hyperactivity (65%) & hypersexuality (50%)
• Incidence: 9%; prevelance: 0.83-22.2%;
• RISK factors: prolonged PTA; seizures;
multifocal lesions; frontal lesions;
orbitofrontal lesions; non-dominant
hemisphere lesions
Kim et al., J Neuropsych Clin Neurosci 2007; 19:106-127
Post-HI Mania
• If frontal injuries: disinhibition & silliness, so
may be hard to distinguish
• Associated with aggression
Post-HI PTSD
• Emotional reactivity common; intrusive
memories rare
• Incidence: 13-27%; prevalence: 3-59%
• RISK factors: loss of consciousness; avoidance
of coping; female; early post-HI depression &
anxiety; L temporal lesions; recall of injury
Kim et al., J Neuropsych Clin Neurosci 2007; 19:106-127
Post-HI Aggression
• Incidence: 34-38%; prevalence: 20-40%
• RISK factors: injury severity; pre-injury
aggression or substance abuse; more than one
injury with loss of consciousness
Kim et al., J Neuropsych Clin Neurosci 2007; 19:106-127
Aggression
• Pre-morbid factors?
• Exclude seizures (early, sudden, bizarre,
stereotypical, no triggers)
• Subdural haematoma
• Pain
• Infections
• Medication
• Alcohol & drugs
• Psychiatric disorders
Personality Disorder
• Causes most distress to all
• Increase in PDs, all types inc. boderline, avoidant, paranoid,
antisocial
• Commoner after frontal damage- dysexecutive syndome
• Orbito-frontal lobes: social behaviour problems, impulsive,
disinhibited, distractible, hyperactive, intolerant, labile mood
• Dorso-lateral frontal lobes: apathy, slowness, perseverative ,
decreased libido
• Correlates with cognitive impairment, but can get normal
memory tests & IQ
• Pre-morbid personality exaggerated
Neuropsychiatric Pharmacological
Interventions
• Little evidence-based
• “hypothesis-driven” management
• Explicit measures/targets at outset to establish
baseline
• Measureable outcomes
• Time limited intervention
• Adequate time & doses
• Adverse effects are more common-inc. cognitive
• Follow principles: “start low, go slow, reach the
top, if you must!”
Some tips.
• Detailed history will often solve a conundrum-get informant
reports and ALL (inc. archives) you can get hold of.
• Include a detailed “medical” history
• What about physical examination?: Be guided by the history.
You can’t meaningfully do a “comprehensive” CNS
examination
• Request investigations based on your hypothesis; some
requests may be to rule out possible causes but these are
usually negative
• A second assessment will give confidence to your formulation
& help in the therapeutic process
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Drugs To Use With Caution
• Anticholinergics (disorientation & memory
problems)
• Short acting “PRN” BZs; regular longer acting
better (avoids withdrawal, addiction,
reinforcement of maladaptive behaviours);
also paradoxical effects
• Drugs that may produce extra-pyramidal S.E.s
• Lower seizure threshold
• Drugs likely to cause drug-interactions
Post-concussion syndrome (PCS)
• Commonest psychiatric disorder
• Validity as a syndrome questioned-as little clustering of
symptoms & resolution unpredictable
• “post-concussion symptoms”-better?
• Mild TBI ≠ PCS; PCS is caused by TBI of any severity
• Mild TBI: 1% to 20%, late symptoms >1yr
• Can be very disabling
• Cognitive, behavioural/emotional, physical symptoms
Severity-Mild TBI
• GCS at 30 min after injury, 13-15
• Duration of PTA <24 hours
• LOC, < or =30 mins
Not always known
•A period of LOC
•Loss of memory (before or
after)
•Alterations in mental state
@injury
•Focal CNS sign
American Congress of Rehabilitation Medicine, 1993
PCS symptoms
• Cognitive: attention, slowed thinking,
memory, executive
• Emotional/behavioural: irritability,
depression, anxiety, affective lability, apathy,
impulsivity
• Physical: headaches, dizziness, fatigue, visual
disturbances, increased sensitivity to noise,
sexual dysfunction, sleep disturbance
Factors underlying PCS
• Pre-injury factors: personality, h/o or F.H. of
psychiatric disorders (inc. alcohol)
• Injury factors: site and extent of damage
• Post-injury factors: epilepsy, psychological
response to HI (e.g. control locus), relationship
& social issues, medico-legal issues
PCS-evaluation-1
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Collateral history important
Detail the symptoms and evolution
Full history essential
Previous TBI will influence outcome
Alcohol & substance misuse-poorer outcome
All factors need to be considered inc. pre-morbid factors-may be
exacerbated with TBI & present with atypical features
• Gradual onset (immediate) and improving over time
• If onset wks or months after TBI & then: (A) symptoms that
worsen or (B) symptoms not in proportion with
neuropsychological tests or neuroimaging-then think of other
causes
PCS-evaluation-2
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Full physical examination
CNS-primitive reflexes & soft neurological signs
MSE
Cognitive tests-focus on attention, speed of information
processing, memory encoding & retrieval, executive
functions, pre-morbid IQ estimates
• ACE-R; FAB (frontal assessment battery)
• Neuroimaging/EEG-supporting evidence of nature &
degree of injury or help explain type of symptoms- not
meant to be diagnostic
• An absence of evidence even if significant TBI, is possible as
techniques not sensitive enough
Differentials in PCS
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Other psychiatric conditions (inc PTSD)
Sleep disorders
Pain
Neurological conditions
Drug- side effects
Relationship issues
Financial issues
Occupational issues
Compensation issues
Anderson et al., 2006; 6:342-357
Anderson et al., 2006; 6:342-357
Anderson et al., 2006; 6:342-357
Anderson et al., 2006; 6:342-357
PCS outlook in Mild TBI
After TBI
3-months
3-6 months
>3-6 months
80-100% -headaches, memory,
attention, slowed thinking
50%-gradual, incomplete recovery
40%-persistence of symptoms
1-20% -some symptoms
Compensation
• Malingering is rare-should only consider if
very good evidence from neuropsychological
tests or inconsistence between level of
functioning and reported symptoms
• Primary or secondary gain is rare
Treatment of PCS-1
• Treat any co-morbid psychiatric conditions
(substance misuse, anxiety, depression, PTSD,
psychosis)
• Treat any co-morbid medical conditions
(seizures, pain, vestibular problems)
• Psycho-education-to all involved
• Goal-directed, step-by-step, individualised,
collaborative approach
Treatment of PCS-2
• Neuropsychological & non-pharmacological
approaches to help with cognitive problems
have been tried with some success in select
cases only; CBT, group therapy, education,
memory aides
• Pharmacological treatments are limited by
lack of approved drugs and limited quality
evidence
Treatment of PCS-3
Cognitive impairment may be explained by
neuromodulator disturbances (unusually a
decrease in function)
• Cholinergic dysfunction
• NE; E; DA-attention, memory, executive
dysfunction
• Attempt to boost levels
Treatment of PCS-4
• Methylphenidate: attention, speed of
processing, arousal; other effects: improved
mood disturbance, aggression (&without
cognition improvements); no dependence or
seizures
• Dextroamphetamine: similar to above
Treatment of PCS-5
Dopamine agonists: improve attention,
arousal, executive function, apathy
• Amantadine: agitation, aggression, affective
liability
• Bromocriptine
• L-dopa/carbidopa
Treatment of PCS-6
Cholinesterase inhibitors
• Attention and memory (acute and late)
• Donepezil
Treatment of PCS-6
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Cytidine 5’-diphosphocholine (CDP-choline)
Enhances activity of AD, NE, Ach
Other effects on phospholipids
Improved general & cognitive symptoms in
trials-inc memory
Not licenced
Treatment of PCS-7
• No clinical measure of neuromodulator
function
• Some patients need more than one type of
agent
• Stimulants: attention, apathy, fatigue,
hypoarousal, low mood (be aware sleep
disturbance as S.E.)
• Cholinesterase inhibitors: memory
Treatment of PCS-Emotional disturbances
• SSRI: depression, irritability, emotional lability
(sertraline has shown benefit)
• SSRI: affective lability (paroxetine, citalopram);
avoid antimuscarinic agents; note response
expected to be quicker than in depression
• Tricyclics: (nortriptyline, desipramine)-may be
beneficial for mood, but avoid as lower seizure
threshold
• Anticonvulsants: (preferred to Lithium)-mania,
irritability, aggression
• Propanolol: aggression, clinical trials
Treatment of PCS-Physical Symptoms
• Headaches -work with neurologists (eg migraine,
root compression)
• Dizziness (anticholnergics are used but may
impair cognition)
• Sleep disturbance (trazadone, avoid BZs, sleep
hygiene)
• Fatigue (stimulants, amantadine; modafinil; may
need to add to those treated for depression)
• Anticonvulsants may target a range of symptomsheadaches, pain, sleep disturbance
References
Fleminger, Head Injury, In: Lishman's Organic Psychiatry: A Textbook of
Neuropsychiatry-4th Edition
Silver, Hales, Yudofskey, Neuropsychiatric aspects of Traumatic Brain Injury,
In: Textbook of Neuropsychiatry and Behavioral Neurosciences-5th
Edition