Group D:HazirahZakwanSheena

SakeenahAmirul

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Common causes and classification of head injury. Levels of impairment of consciousness. Acute psychological sequelae:

◦ Post-traumatic amnesia Chronic psychological sequelae:

◦ Lasting cognitive impairment◦ Post-concussional syndromes◦ Personality change◦ Emotional disorder and Schizophrenia-like syndromes◦ Social consequences of head injury

Management of head injury

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• Also known as acquired brain injury, head injury, traumatic brain injury (TBI), or brain injury, causes substantial disability and mortality.

• It occurs when a sudden trauma damages the brain and disrupts normal brain function.

• TBI may have profound physical, psychological, cognitive, emotional, and social effects.

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Falls (28%) Motor vehicle crashes (20%) Being struck by or against objects (19%) Assaults (11%)

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Primary injury Secondary injury

Related to tissue impairment which results directly from the impact forces

Developed subsequently as tissue response to the primary injuries or systemic events.

Localized-laceration of brain parenchymaDiffuse-Diffuse axonal injury

Inflammation,ischaemia

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Classification

IntracranialFocal• Epidural• Subdural• Intracerebral / Contusion

Diffuse• Mild concussion• Classic concussion• Diffuse axonal injury

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Scales and terms to classify the levels of consciousness differ

reduction in response to stimuli = decreasing level of consciousness

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Level Summary Description

Conscious Normal Assessment of LOC involves checking orientation: •people who are able promptly and spontaneously to state their name, location, and the date or time are said to be oriented to self, place, and time, or "oriented X3"•A normal sleep stage from which a person is easily awakened is also considered a normal level of consciousness.•"Clouding of consciousness" is a term for a mild alteration of consciousness with alterations in attention and wakefulness.

Confuse Disoriented; impaired thinking and responses

People who do not respond quickly with information about their name, location, and the time are considered "obtuse" or "confused".A confused person may be bewildered, disoriented, and have difficulty following instructions. The person may have slow thinking and possible memory time loss. This could be caused by sleep deprivation, malnutrition, allergies, environmental pollution, and infection.

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Delirious Disoriented; restlessness, hallucinations, sometimes delusions

Some scales have "delirious" below this level, in which a person may be restless or agitated and exhibit a marked deficit in attention

Somnolent SleepyA somnolent person shows excessive drowsiness and responds to stimuli only with incoherent mumbles or disorganized movements.

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Obtunded

Decreased alertness; slowed psychomotor responses

In obtundation, a person has a decreased interest in their surroundings, slowed responses, and sleepiness.

Stuporous

Sleep-like state (not unconscious); little/no spontaneous activity

People with an even lower level of consciousness, stupor, only respond by grimacing or drawing away from painful stimuli.

Comatose

Cannot be aroused; no response to stimuli

Comatose people do not even make this response to stimuli, have no corneal or gag reflex, and they may have no pupillary response to light.

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Post-traumatic amnesia

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state of confusion that occurs immediately following a traumatic brain injury (TBI) ◦ disoriented and unable to remember events that occur after the

injury. unable to state his or her name, where he or she

is, and what time it is. While PTA lasts, new events cannot be stored in

the memory. About a third of patients with mild head injury are

reported to have "islands of memory", in which the patient can recall only some events.

During PTA, the patient's consciousness is "clouded".

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Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "posttraumatic confusional state" has been proposed as an alternative.

When continuous memory returns, PTA is considered to have resolved.

There are two types of amnesia: ◦ retrograde amnesia (loss of memories that were

formed shortly before the injury)◦ anterograde amnesia (problems with creating

new memories after the injury has taken place).

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PTA has been proposed to be the best measure of head trauma severity, but it may not be a reliable indicator of outcome.◦ PTA duration may be linked to the likelihood that psychiatric

and behavioral problems will occur as consequences of TBI. Classification systems for determining the

severity of TBI may use duration of PTA alone or with other factors such as Glasgow Coma Scale (GCS) score and duration of loss of consciousness (LOC) to divide TBI into categories of mild, moderate, and severe. ◦ Duration of PTA usually correlates well with GCS and usually

lasts about four times longer than unconsciousness.

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PTA is considered a hallmark of concussion, and is used as a measure of predicting its severity, for example in concussion grading scales. ◦ It may be more reliable for determining severity of concussion

than GCS because the latter may not be sensitive enough; concussion sufferers often quickly regain a GCS score of 15.

Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms from concussion.◦ Increased duration of PTA is associated with a heightened risk

for TBI complications such as post-traumatic epilepsy.

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Levels of TBI severity

  GCS PTA LOC

Mild 13–15<1

hour

<30minute

s

Moderate

9–12

30 minute

s–24

hours

1–24hours

Severe 3–8>1 day

>24hours

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TBI severity using PTA alone

Severity PTA

Very mild < 5 minutes

Mild 5–60 minutes

Moderate 1–24 hours

Severe 1–7 days

Very severe 1–4 weeks

Extremely severe

> 4 weeks

•LASTING COGNITIVE IMPAIRMENT•POST-CONCUSSIONAL SYNDROMES

•PERSONALITY CHANGE•EMOTIONAL DISORDER AND

SCHIZOPHRENIA-LIKE SYNDROMES •SOCIAL CONSEQUENCES OF HEAD

INJURY

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1.Lasting cognitive impairment2.Post- concussional

syndromes3.Personality change4.Emotional disorder and

schizophrenia-like syndromes

5.Social consequences of head injury

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Cognitive deficits: Impairment in efficiency and speed of information processing, attention and vigilance are seen in most cases. Alertness is impaired in severe TBI. The patient may be withdrawn, dull, and apathetic. Deficit of alertness often accompany deficits of motivation. Divided attention deficits are present

Memory: Newly acquired knowledge is forgotten. Selective impairement of memory may persist

depending upon the circumscribed damage to structures in

diencephalon or medial temporal lobe structures. Both recent and remote memory may be impaired, but immediate memory may be spared

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Perception: Visual dysfunction affects about 50% of TBI patients. Visuo-perceptual disturbances such as impaired figure-ground perception and constructional abilities may be present in severe TBI as part of a

general cognitive decline. Focal visuo-perceptual and

visuoconstructive disabilities are rare.

Language: Anomia and word finding difficulties are present after TBI. Expressive aphasias are more common than receptive aphasias. TBI patients with aphasias have more severe cognitive deficit compared to those patients without aphasia. Recovery from

aphasia and related language disorder is greater than recovery from memory and other cognitive deficits when patients were tested after one year

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Intelligence: Both performance and verbal IQ are reduced in acute and chronic phases of severe TBI. Recovery of verbal IQ is faster. Performance IQ continued to be lower even after three years. 10% of TBI patients with prolonged coma develop some

degree of hydrocephalus, which may present as progressive intellectual deterioration.

Factors predisposing to the development of posttraumatic

dementia include severity of head injury,multiplicity of head trauma, age greater than 60 years,alchoholism and atherosclerosis.

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PCS often follows mild TBI. Onset of PCS is usually during the first month

after TBI, and may slightly reduce after 3-6 months, though a significant

percentage continue to be symptomatic. PCS

Patients have reduced blood flow through the brain as well as prolongation

of mean cerebral circulation time. Abnormal audiologic examination has

been reported in PCS patients complaining of dizziness, hearing disturbance and tinnitus.

PET has demonstrated changes in cerebral glucose metabolism greater

than would be expected by the lesions detected by CT and MRI scans..

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

Note: the manifestations of concussion include loss of consciousness, posttraumatic amnesia, and, less commonly posttraumatic onset of seizure. The specific method of defining this criterion needs to be established by further research

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

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

(1) Becoming fatigued easily(2) Disordered sleep(3) Headache(4) Vertigo or dizziness(5) Irritability or aggression on little or no

provocation(6) Anxiety, depression, or affective lability(7) Changes in personality (eg: social or sexual

inappriopriateness(8) Apathy or lack of spontaneity

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D. The symptoms on criteria B and C have heir onset following head trauma or else represent a substantial worsening of preexisting symptoms

E. The disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning. In school-age children, the impairment may be manifested by a significant worsening in school or academic performance dating from the trauma

F. The symptoms do not meet criteria for dementia due to head trauma and are not better accounted for by another mental disorder (eg: amnestic disorder due to head trauma, personality change due to head trauma)

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Common symptoms of the post concussion syndrome

1. Somatic symptoms Headache Dizziness Fatigue2. Cognitive symptoms Memory difficulties Impaired concentration3. Perceptual symptoms Tinnitus Sensitivity to noise Sensitivity to light4. Emotional symptoms Depression Anxiety Irritability

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Alyman(1999):no relationship between maladaptive personality characteristics

Hoffman, Scott, Emick, and Adams (1999), Youngjohn,Davis, and Wolf (1997): personality is more strongly related to legal issues than the injury

Fordyce,Roueche, and Prigatano (1983): chronic head injured patients were more anxious and depressed than those with acute head injuries.

Marcelli and Temey (1977):there is a psychopathological core common to all closed head trauma cases, which result in prolonged coma.

Miller and Donders (2001) attempted to evaluate the impact of injury severity on personality change using the MMPI: they found that individuals with mild TBI had more personality problems than those with more severe problems. However, they also found out that...

MMPI was more strongly related to financial (legal) issues more than aspects of head injury

MMPI: Minnesota Multiphasic Personality Inventory

TBI: traumatic brain injury

Landry (1997): length of coma was positively correlated with scores on the Minnesota Multiphasic Personality Inventory (MMPI) scales.

There is no specific way of measuring how severe the head injury- Length of time LOC- Residual cognitive result, Halstead-Reitan Neuropsychological Battery (HNRB)

Head injury to the orbito-frontal lobe or anterior temporal lobe

‘Frontal lobe syndrome’Disinhibition(reduced capacity to edit or manage their

immediate impulsive response to a situation)Impulsivity(act on impulse rather than thought)IrritabilityAggressive outburstsTx:ß-blockers(eg.atenolol), carbamazepine

Test frontal lobe function:I. Frontal assesment battery(FAB)

maximum score is 18 Below 17 indicates frontal lobe impairment

II. The wisconsin card sorting task(tests response inhibition and set shifting)

Det the card allocation and allocate card accordingly Frontal lobe impairment will make more errors

III.Digit span(short term verbal memory) Forward, normal max 6±1 Reverse order, normal max 5±1

IV.Trail making test-join the dots(visuomotor) Simple number sequence Alternating numbers and letters

V. Cognitive estimate testing Ask question that requires abstract reasoning and cannot

be answered by general knowledge alone

Emotional disorder extent of psychological trauma

Schizophrenia-like syndromes Paranoia is associated with left temporal

injury Affective psychoses(esp.mania in 9 %

patients) are associated with right temporal/orbito-frontal injury

prevelence is about 2.5% Treatment: antipsychotics, anticonvulsant

Clinical symptoms of post-traumatic psychosis Delusions (usually persecutory) Achte et al. (1991): delusional psychosis occurs at

twice the frequency of post-traumatic schizophrenia-like psychosis(28% and 14%, respectively).

Fujii and Ahmed(2002): Among patients with post-traumatic delusions, persecutory (38%), grandiose (15%), and/or somatic (15%) types were most common.

Similarly, Sachdev et al. (2001): persecutory (56%), referential (22%), control (22%), grandiose (20%), and/or religious(15%) delusions are the most common types among persons with post-traumatic psychosis.

Hallucination Fujii & Ahmed,(2002): auditory(92%) rather

than visual (32%) Fujii & Ahmed,(2002): Subjects with relatively

later onset of psychosis (> two years following TBI) are more likely to experience hallucinations than those with earlier onset. Among subjects with relatively earlier onset of psychosis, visual hallucinations are more common than auditory hallucinations.

combinations of delusions and hallucinations (i.e., ‘schizophreniform’ or ‘schizophrenia-like’ conditions)

Disturbances of thought process and ‘negative’symptoms are neither necessary nor sufficient for thediagnosis of post-traumatic psychosis. Deficit type symptoms (anhedonia, lack of

spontaneity, and loss of social contact) may occur Sachdev et al., (2001): such symptoms are less

common and less prominent than post traumaticn delusions and hallucinations

Fujii & Ahmed, (2002).: such symptoms are substantially less common than in schizophrenia

Post-traumatic neurocognitive disturbances may mimic the disturbances of thought and behavior of schizophrenia and may be mistaken as such if

not otherwise identified properly. Some of the posttraumatic aphasias resemble superficially the disturbed thought process of schizophrenia, including:

non-fluent speech with agrammatical (‘disorganized’)

structure and undue word finding pauses(‘alogia’ and/or ‘thought blocking’).

Word substitutions,phonemic paraphasias, and/or neologisms may result in apparently ‘disorganized’ speech (or even jargon aphasia akin to ‘word salad’),

Adjustment to disability Ability to play a variety of social role Ability t maintain social relationship Quality of life

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• Family relationships are significantly altered

– Prolonged stress of caregiver– Financial burden• Neither the family nor the individual has theopportunity to prepare for the emotional andeconomic impact of TBI

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Aim help patient achieve optimum level of functioning.

The level of disability at various stages following the injury needs to be assessed clearly

Important to keep the family members informed about his clinical status and the level of disability.

Domains of management: RehabilitationPharmacological intervention

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Encompasses cognitive rehabilitation, behavioral treatment, social skills training, vocational training, individual therapy, group therapy, and family therapy.

Rehabilitation should begin on the day of the injury and continue until the patient is stable or has recovered fully.

Appropriate period of rest away from work is necessary depending upon the severity of injury and complications

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Functional skill development is the hallmark of cognitive retraining programs.

Each patient’s disability is analyzed.

A therapist helps the patient to structure tasks, which is encountered in day-to-day life.

Strategies are thought to overcome the deficits of the patient.

Functional skill development is a useful approach in rehabilitation of the head injured patients.

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Personality changes are often resistant to treatment.

Psychotherapy at superficial levels may help.

Behavioral techniques like social skills training may help in reducing disruptive behaviors.

Operant conditioning by rewarding self-helping behaviour.

Relaxation training is useful in anxiety disorders.50

A particularly important part of patient’s recovery.

The most stress for relatives of head injury patients occur in 1-6 months.

The patient’s disability may inflict social isolation on the family.

Families need reassurance that anger, frustration and sorrow are natural emotional reaction for caregivers.

Organizing self-help groups, educating the family in handling the patient, providing trained helpers will help in rehabilitation

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To treat seizure disorder, mood lability, mania, impulsivity, aggression, and rage

Carbamazepine and valproic acid are most commonly used + equally beneficial.

Phenytoin and barbiturates are not recommended decrease cognitive function and motor performance.

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SSRIs are useful in the treatment of depression, mood lability and impulsivity.

TCAs and MAOIs not preferred anticholinergic side effects and drug–food interactions, respectively.

Trazodone (anti-depressant) is useful for agitation and sleep (off-label use).

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Psychostimulants (e.g. Methylphenidate) are useful in:

Inattention Distractibility Disorganization Hyperactivity Impulsivity Hypoarousal Apathy Hypersomnia Mood and cognition

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Head injury is frequently associated with disturbances of dopamine transmission & persisting for many years.

The frontal lobes are rich in dopamine & their frequent involvement in head injury is associated with decreased dopamine activity.

Amantadine, bromocriptine, and levodopa have been used in the treatment of cognitive symptoms

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Zolpidem is a non-benzodiazepine hypnotic indicated for short-term management of insomnia with a rapid onset and short half-life (2-3 hours)

Zopiclone is a longer acting alternative.

Trazodone (less anticholinergic side effects and little cardiotoxicity) is frequently used as a hypnotic because of its sedative properties and its physiological effects on slow wave sleep.

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Naltrexone (opiod-receptor antagonist) is useful in treating self-injurious behavior.

Buspirone, a postsynaptic serotonin -1A partial agonist is also useful in the treatment of aggression.

Beta-blockers e.g. propranolol have also been used to treat aggression and violent behavior.

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