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POST CONCUSSION SYNDROMEC/P : DR.JOHN MATHAIPRESENTER:DR.DAVIN10/08/2011

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INTRODUCTIONPossible outcome of mild

Traumatic Brain Injury(mTBI)(GCS NOT < 13)

Post concussional symptoms seen in 38%-80% of people with mTBI

Post Mortem studies showed Diffuse axonal injury.

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SYNONYMSPostconcussional disorder(DSM

IV)Post traumatic brain

syndrome,nonpsychoticShell shockPosttrauma concussion statePosttrauma syndrome

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HISTORYErichsen(1866)-complaints were

due to trauma induced “molecular disarrangement” of spinal cord.(“railroad spine”)

Rigler(1879)-proposed injuries were due to “compensation neurosis”

Charcot-due to “hysteria and neurasthenia”

World war I – “shell shock”

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HISTORY1939-Coined “posttrauma

concussion state” to avoid epidemic of “shell shock” cases

Disturbance of consciousness with no immediate/obvious pathologic change in the brain

1941- POST CONCUSSION SYNDROME

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Lewis(1942) about PCS“That common dubious

psychopathic condition – the bugbear of the clearminded doctor and lawyer”

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DEFINITION“Rarely Clearly Defined”A condition arising after “head injury”

that produces deficits in 3 areas of CNS functioning:

1) Somatic(neurological-headache,fatigue)

2) Psychological(affective change,lack of motivation,anxiety,emotional lability)

3) Cognitive (impaired memory,attention,concentration)

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EPIDEMIOLOGYIndia - >1 million sustain head

injuries/year80-90% -minor head injuries50% have post concussive

symptoms at 1 month,15% at end of 1 year.

Morbidity – mainly persistent symptoms

Sex-Incidence more in females(US)

Age – 50% between ages 15-34(US)

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ETIOLOGY

A. Brain injuryMicroscopic lesions in brain post

mortem – diffuse axonal injury,microglial clusters,small petechial hemorrhages.

Imaging (Functional with single photon emission CT or PET) show abnormalities – SPECT showed decreased or asymmetric regional blood flow upto 3 years later.

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ETIOLOGYPET scans-reduced metabolic

rate of glucose utilization-documentation for malingering.

Evidence of cerebral dysfunction after mild head injury – a working memory task showed more widespread activation of cerebral cortex though performance was normal

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ETIOLOGY

B. Psychological factorsMostly seen in symptoms lasting

> 1 yearMore likely if patient blames

employerCompensation claims increase

symptoms by about 25%Role is greatest in very mild

injuries and very chronic symptoms

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ETIOLOGYC. Model of interactionProposed by Lishman(1988)Most patients-good recoveryPsychological effects interfere with

normal recovery process – PCS developsAnxiety – patient worries about

symptoms,focuses on them Aggravated – compensation issues and

vulnerability to somatizationVicious circle of disability-anxiety-

symptoms.

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CLINICAL FEATURESEssential FeatureAcquired impairment in cognitive

functioning , with specific neurobehavioural symptoms as a consequence of closed head injury of sufficient severity to produce significant cerebral concussion.

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CLINICAL FEATURESManifestations of concussion

include:1. Loss of consciousness > 5 min2. Posttraumatic amnesia >12 hrs3. New onset/worsening of seizures

within first 6 months

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SOMATIC HeadacheMost common(30-90%)Last longer , occur more frequently than

before the injuryIHS criteria divides into:Acute –within 2 wks,resolve by 2 mthsChronic –within 2 wks ,continue >8 wks85% -steady,aching,tension-typeDue to soft and hard tissue injuriesMigraines –common in

adolescents,sportspeople

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SOMATICDizzinessReported in 50% , 1 yr

prevalence-19-25%Balance uncertainty,LightheadednessSubjective unsteadiness of gaitOlder age correlates for likelihood

of dizzinessDifferentiate from true vertigo

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SOMATICBlurred vision 14%-optical

convergence disorderPhonophobia,photophobia-

10%Decreased smell and taste

~5%Sleep problems – onset and

maintainence

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PSYCHOLOGICALAnxietyNearly 50% report personality

change,irritability,anxiety or depression within 3 months

Anxiety disorders include Generalised anxiety disorder,panic disorder,OCD,PTSD-(11-70%)

Most common-free floating anxiety , fearfulness, intense worry ,social withdrawal

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PSYCHOLOGICALApathyCan be primary(10%) or

secondary to depression(~60%)Neurological damage to

subcortical-frontal region,basal ganglia and thalamus –primary apathy

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PSYCHOLOGICALPsychosisExtremely rare Risk factors – severity of trauma ,

h/o temporal lobe epilepsy , head trauma during adolescence

Atypical antipsychotics better for treatment

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PSYCHOLOGICALPreexisting affective disorders

can result in misdiagnosis of PCS as symptoms of mood change,lability,sleep disturbances,anxiety overlap.

Recall biases – “good old days”phenomenon

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COGNITIVEReductions in information

processing , attention, reaction timeNeuropsychological tests : predict

durationStroop color testProcessing speed testContinuous performance test of

attentionDigit span forwardHopkins verbal learning test

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COGNITIVEVerbal and non verbal memory

impairment –most common(20-79%)

Short term memory deficits – “effortful”> “incidental”

Impaired sustained and divided attention-due to cholinergic dysfunction-impaired sensory gating

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DIAGNOSISDCR 10ICD 10DSM IV

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DCR 10A. The general criteria of F07

must be met.B. History of head trauma with

loss of consciousness, preceding the onset of symptoms by a period of upto four weeks (objective EEG, brain imaging, or oculonystagmographic evidence for brain damage may be lacking).

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DCR 10

C. At least three of the following:(1) Complaints of unpleasant sensations

and pains, such as headache, dizziness (usually lacking the features of true vertigo), general malaise and excessive fatigue. or noise intolerance.

(2) Emotional changes, such as irritability, emotional lability, both easily provoked or exacerbated by emotional excitement or stress, or some degree of depression and/or anxiety.

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DCR 10(3) Subjective complaints of

difficulty in concentration and in performing mental tasks, and of memory complaints, without clear objective evidence (e.g. psychological tests) of marked impairment.

(4) Insomnia.(5) Reduced tolerance to alcohol

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DCR 10(6) Preoccupation with the above

symptoms and fear of permanent brain damage, to the extent of hypochondriacal over-valued ideas and adoption of a sick role.

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ICD - 10F07.2 Postconcussional syndromeOccurs following head

trauma(usually sufficiently severe to result in loss of consciousness)

At least 3 of following symptoms:1. Headache2. Dizziness3. Fatigue4. Irritability

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ICD - 10

5. Difficulty concentrating , performing mental tasks

6. Memory impairment7. Insomnia8. Reduced tolerance to stress

emotional excitement or alcohol

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ICD - 10Feelings of anxiety or depression –loss of

self esteem and fear of permanent brain damage.

Hypochondriacal Nosological status uncertain“Common and distressing to patient”Includes:1. Postcontusional

syndrome(encephalopathy)2. Post-traumatic brain syndrome ,

nonpsychotic

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DSM IV TR

A. A history of head trauma that has caused significant cerebral concussion.

B. Evidence from neuropsychological testing or quantified cognitive assessment of difficulty in attention(concentrating,shifting focus of attention,performing simultaneous tasks) or memory(learning or recalling information).

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DSM IV TR

C. Three (or more) of the following occur shortly after the trauma and last at least 3 months:

1. Becoming fatigued easily2. Disordered sleep3. Headache4. Vertigo or dizziness5. Irritability or aggression on little

or no provocation

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DSM IV TR

6. Anxiety,depression or affective liability

7. Changes in personality(e.g. social or sexual inappropriateness)

8. Apathy or lack of spontaneity.D. The symptoms in criteria B and C

have their onset following head trauma or else represent a substantial worsening of preexisting symptoms.

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DSM IV TR

E. Causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning.

F. Do not meet criteria for Dementia due to Head Trauma and are not better accounted for by another mental disorder.

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DIFFERENTIAL DIAGNOSISMild neurocognitive

disorder(specific etiology and symptoms)

Somatisation disorder,undifferentiated somatoform disorder

Factitious disorder,malingeringPTSDAffective disordersChronic fatigue syndrome

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INVESTIGATIONSCT Scan – to r/o intracranial

abnormalities and skull fractures.Functional MRI,SPECT,PET – more

sensitive for minor head injuriesEEG - epilepsyNeuropsychological testing.

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TREATMENTDepends on specific symptoms

constellationEducate patient and family about

PCS , recovery period Lack of knowledge worsens

psychogenic symptoms and prolongs recovery time

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TREATMENTPersistent headaches-

NSAIDS,migraine prophylactics ( fluoxetine) helpful.

Psychological symptoms-supportive psychotherapy , education, pharmacotherapy for a limited time.

SSRIs are antidepressants of choice –relieve headache,anxiety,tension,depression

Memory deficits-Mild benefits from meds

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TREATMENTAvoid phenytoin , haloperidol,

barbiturates due to significant side effects like

Delayed neuronal recovery,Paradoxical rage,Memory impairmentIndian studies (Deepak et

al ,2007)-Piracetam useful

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COURSE AND PROGNOSISGenerally very good to excellentMost cases –symptoms resolve within

few days to weeksMost are symptom free by 3 months~10 % -symptoms persist more than a

year-leads to persistent PCS(PPCS)Anxiety and depression often the cause

for persisting symptomsRequire multidisciplinary cognitive

therapy programs including vocational training.

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CONTROVERSIESNumerous symptoms in different fields

with no clear association among them-Syndrome?

Each symptom can have specific diagnosis e.g. dizziness-BPPV,headache-migraine

Cause not exactly known-psychogenic or physiogenic

Lishman proposed physiogenic-organic influences and psychogenic –long lasting symptoms

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THANK YOU

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