You are on page 1of 45

POST CONCUSSION SYNDROME

C/P : DR.JOHN MATHAI PRESENTER:DR.DAVIN 10/08/2011

INTRODUCTION
Possible 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.

SYNONYMS
Postconcussional disorder(DSM IV) Post traumatic brain syndrome,nonpsychotic Shell shock Posttrauma concussion state Posttrauma syndrome

HISTORY
Erichsen(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

HISTORY
1939-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

Lewis(1942) about PCS That common dubious psychopathic condition the bugbear of the clearminded doctor and lawyer

DEFINITION
Rarely Clearly Defined A condition arising after head injury that produces deficits in 3 areas of CNS functioning: 1) Somatic(neurologicalheadache,fatigue) 2) Psychological(affective change,lack of motivation,anxiety,emotional lability) 3) Cognitive (impaired

EPIDEMIOLOGY
India - >1 million sustain head injuries/year 80-90% -minor head injuries 50% 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)

ETIOLOGY
A.

Brain injury Microscopic 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.
9

ETIOLOGY
PET 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

10

ETIOLOGY
B.

Psychological factors Mostly seen in symptoms lasting > 1 year More likely if patient blames employer Compensation claims increase symptoms by about 25% Role is greatest in very mild injuries and very chronic symptoms
11

ETIOLOGY
C.

Model of interaction Proposed by Lishman(1988) Most patients-good recovery Psychological effects interfere with normal recovery process PCS develops Anxiety patient worries about symptoms,focuses on them Aggravated compensation issues and vulnerability to somatization Vicious circle of disability-anxietysymptoms.

12

CLINICAL FEATURES
Essential Feature Acquired impairment in cognitive functioning , with specific neurobehavioural symptoms as a consequence of closed head injury of sufficient severity to produce significant cerebral concussion.

13

CLINICAL FEATURES
Manifestations of concussion include: 1. Loss of consciousness > 5 min 2. Posttraumatic amnesia >12 hrs 3. New onset/worsening of seizures within first 6 months

14

15

SOMATIC
Headache Most common(30-90%) Last longer , occur more frequently than before the injury IHS criteria divides into: Acute within 2 wks,resolve by 2 mths Chronic within 2 wks ,continue >8 wks 85% -steady,aching,tension-type Due to soft and hard tissue injuries Migraines common in adolescents,sportspeople

16

SOMATIC
Dizziness Reported in 50% , 1 yr prevalence-1925% Balance uncertainty, Lightheadedness Subjective unsteadiness of gait Older age correlates for likelihood of dizziness Differentiate from true vertigo

17

SOMATIC
Blurred vision 14%-optical convergence disorder Phonophobia,photophobia-10% Decreased smell and taste ~5% Sleep problems onset and maintainence

18

PSYCHOLOGICAL
Anxiety Nearly 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

19

PSYCHOLOGICAL
Apathy Can be primary(10%) or secondary to depression(~60%) Neurological damage to subcorticalfrontal region,basal ganglia and thalamus primary apathy

20

PSYCHOLOGICAL
Psychosis Extremely rare Risk factors severity of trauma , h/o temporal lobe epilepsy , head trauma during adolescence Atypical antipsychotics better for treatment

21

PSYCHOLOGICAL
Preexisting affective disorders can result in misdiagnosis of PCS as symptoms of mood change,lability,sleep disturbances,anxiety overlap. Recall biases good old daysphenomenon

22

COGNITIVE
Reductions in information processing , attention, reaction time Neuropsychological tests : predict duration Stroop color test Processing speed test Continuous performance test of attention Digit span forward Hopkins verbal learning test

23

COGNITIVE
Verbal 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

24

DIAGNOSIS
DCR 10 ICD 10 DSM IV

25

DCR 10
A. 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).

26

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.

27

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

28

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.

29

ICD - 10
F07.2 Postconcussional syndrome Occurs following head trauma(usually sufficiently severe to result in loss of consciousness) At least 3 of following symptoms: 1. Headache 2. Dizziness 3. Fatigue 4. Irritability

30

ICD - 10
5. 6. 7. 8.

Difficulty concentrating , performing mental tasks Memory impairment Insomnia Reduced tolerance to stress emotional excitement or alcohol

31

ICD - 10
Feelings 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

32

DSM IV TR
A.

B.

A history of head trauma that has caused significant cerebral concussion. 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).
33

DSM IV TR
C.

1.

2.
3. 4.

5.

Three (or more) of the following occur shortly after the trauma and last at least 3 months: Becoming fatigued easily Disordered sleep Headache Vertigo or dizziness Irritability or aggression on little or no provocation
34

DSM IV TR
6. 7.

8.
D.

Anxiety,depression or affective liability Changes in personality(e.g. social or sexual inappropriateness) Apathy or lack of spontaneity. The symptoms in criteria B and C have their onset following head trauma or else represent a substantial worsening of preexisting symptoms.
35

DSM IV TR
E.

F.

Causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning. Do not meet criteria for Dementia due to Head Trauma and are not better accounted for by another mental disorder.

36

DIFFERENTIAL DIAGNOSIS
Mild neurocognitive disorder(specific etiology and symptoms) Somatisation disorder,undifferentiated somatoform disorder Factitious disorder,malingering PTSD Affective disorders Chronic fatigue syndrome

37

INVESTIGATIONS
CT Scan to r/o intracranial abnormalities and skull fractures. Functional MRI,SPECT,PET more sensitive for minor head injuries EEG - epilepsy Neuropsychological testing.

38

TREATMENT
Depends on specific symptoms constellation Educate patient and family about PCS , recovery period Lack of knowledge worsens psychogenic symptoms and prolongs recovery time

39

TREATMENT
Persistent headachesNSAIDS,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

40

TREATMENT
Avoid phenytoin , haloperidol, barbiturates due to significant side effects like Delayed neuronal recovery, Paradoxical rage, Memory impairment Indian studies (Deepak et al ,2007)Piracetam useful

41

COURSE AND PROGNOSIS


Generally very good to excellent Most cases symptoms resolve within few days to weeks Most 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 symptoms Require multidisciplinary cognitive therapy programs including vocational training.

42

CONTROVERSIES
Numerous symptoms in different fields with no clear association among themSyndrome? Each symptom can have specific diagnosis e.g. dizzinessBPPV,headache-migraine Cause not exactly known-psychogenic or physiogenic Lishman proposed physiogenicorganic influences and psychogenic long lasting symptoms

43

THANK YOU

44

45

You might also like