Clinical
features:
Post-traumatic headache: Headache, which is
part of the post-concussional syndrome, is often associated with auditory
and vestibular symptoms ± psychoneurotic features. Headache can also be
the predominant symptom following head injury, in a group of people with
no neurological deficit. Trauma appears to have precipitated or
aggravated an underlying headache. The pain is mainly occipito cervical
extending to the vertex. Movement of the head, anxiety, concentration,
effort aggravate the headache. The headache is associated with tension in
the neck muscles. Reflex muscular contraction in the back of the neck may
be due to a whiplash injury. Associated inability to concentrate,
tiredness and insomnia may indicate associated depression, which could
often be the primary cause. There is a good response to antidepressants.
Local pain may occur in an area of scalp bruising due to myalgia of the
underlying muscle, particularly the temporalis muscle. Management
includes reassurance, minor tranquilisers, analgesics and psychotherapy.
It is to be reiterated that post traumatic headache can also be
due to raised intra-cranial pressure. These include chronic
extradural hematoma, chronic subdural hematoma, hygroma, post traumatic
meningitis, pneumocephalus, abscess, venous sinus thrombosis and hydrocephalus.
Post
traumatic dizziness: Rarely
this may be due to a true vertigo due to haemorrhage in the labrynth or
due to damage of the vestibular component of the eighth nerve. Milder
symptoms of labrynthine dysfunction may be associated with fractures of
the petrous temporal bone, often difficult to demonstrate.
Other
Clinical Features:
The duration of PTS is debatable. Concussed subjects reported high levels
of disturbance in affective, cognitive and social functioning even at 3
months. Some patients even report symptoms after one year. Though a
significant impairment may persist for several weeks after the injury,
the trend is towards gradual improvement, which suggests a recovery
process. Higher distress levels are evident among those with minor head
injury compared to severe head injury. PTS is a symptom complex that
includes physical discomfort and disturbances of sleep, sex, affective
and sensory disturbances. There is difference of opinion regarding the
rate and extent of recovery following mild closed head injury. This is
dependent on extent of injuries including head trauma, age, prior
vocational skills, education, cognitive abilities, psychosocial
functioning and general physical health. A prospective study of 60
randomly selected patients with closed head injury from NIMHANS
Bangalore, India revealed neuro-psychiatric disturbances in 80% at 6
weeks. Social dysfunction was directly related to the severity of the
head injury. The total number of symptoms (largely subjective) correlated
with pre traumatic neuroticism. injury related environmental and
personality related factors In one study 34% of previously employed
patients were not working three months after the injury. The degree of
unemployment correlated with either lower soco-economic class or lack of
buffers to minimize stresses at the job site. Although young men are at
the greatest risk of minor head injury, older women appear to be at
increased risk for chronic sequelae.
Etiology:
Postulations
vary from psychogenic to organic. Walpole Levin postulated that symptoms
started as organic and persisted as psychic. Axonal and neuronal damage
in focal areas in the hemisphere, are implicated as the substrate in mild
brain injuries, as contrasted to shearing injuries in the brain stem in severe
injuries. The importance of aggravation of features in post-traumatic
syndrome where compensation is involved suggests a non-organic basis. The
increased occurrence of this syndrome in neurotic patients suggests that
the pre-traumatic personality also has a role to play. Many of
those suffering from PTS appear to be estranged from abusive families.
Pathophysiology
of minor head injury is
difficult to elucidate due to the lack of objective detectable
neurological deficits and unremarkable imaging studies. Pathological
studies are not possible as death never occurs due to the syndrome per
se. The post-traumatic subjective complaints are thought to be
psychosocial than organic. Several studies now document a physiological
etiology though not demonstrable on current imaging studies. Degenerating
axons in the brain stem were found in concussions produced
experimentally. There appears to be a structural basis for concussion
based on prolonged brain stem conduction time.
Investigations:
EEG
studies in 54 patients
with the PTS following minor head trauma revealed paroxysmal activity in
9.2% either specific or non-specific. While being monitored 24 patients
experienced symptoms typical of this disorder without concurrent EEG
abnormalities. No patient exhibited abnormalities in the 24-hour
ambulatory recording. Symptoms of PTS were not epileptogenic in nature.
Tc
HMPAO SPECT
studies in persistent post concussion syndrome after mild head injuries
have been done. SPECT was read as abnormal in 53% of 43
patients and showed a total of 37 lesions. MRI was abnormal in 9% and CT
in 4.6%. SPECT appeared to be more sensitive in detecting cerebral
abnormalities after mild head injury especially in the PTS. No
statistically significant relationship was found between SPECT scan
abnormalities and age, past or present psychiatric problems or
educational levels.
Trigeminal
and auditory evoked responses in post concussion syndrome. 40 patients with
minor head trauma had Brain Stem Trigeminal Evoked Potentials, Brain Stem
Auditory Evoked Potentials and Middle Latency Auditory Evoked Potentials
(MLAEP). Evaluation was done within 48 hours and at 3 months following
trauma. Failure to resume previous professional activity, headache,
memory disorders, dizziness and vertigo, behavioural and emotional
disturbances and other symptoms of a neurological nature were
specifically looked for. PTS was said to exist if four or more
symptoms persisted. All three Evoked Potential modalities showed
significantly increased latencies at the initial assessment, disclosing
disseminated axonal damage. Outcome at 3 months appeared to be correlated
to the MLAEP’s. It is therefore postulated that organic diencephalic
paraventricular primary changes may account for the occurrence of the
PTS.
Hypersensitivity
to light and sound
following minor head trauma has been objectively studied. Mean luminance
(1366 Lux) tolerated by patients with minor head trauma was significantly
lower than that tolerated by controls (1783 Lux). The mean sound intensity
(84 db) was also less than that tolerated by controls (94 db). The
results demonstrate an objective basis for complaints of increasing
sensitivity at least to light following head injury. These findings do
not support earlier psychogenic explanations for the PTS.
Management:
A
survey of the members of the National Academy of Neuropsychology and the
International Neuropsychological Society was conducted on current
treatment approaches for post concussion syndrome.
The
incidence of PTS itself appears less, when all cases of concussion
are admitted to a head injury unit, observed and discharged with
reassurance, encouragement and symptomatic treatment from day 1 .
Thoughtless remarks about brain injury in front of the patient should be
avoided. Anxiety and depression need to be combated.
Education
about the effects of head injury, reassurance that the symptoms were part
of the natural recovery process and support in coping with the reactions
to the symptoms were found most useful. Recreation, inculcating a sense
of human interdependency, and community living were also
recommended.
Group
therapy can be useful in addition to individual therapy Graded resumption
of activity, anti depressant medication and cognitive restructuring were
also found to be useful.
Oxiracetam
and pervincamine have been used. Muscle relaxants and biofeedback have
also been used. The reserve capacities of the brain for
establishment of compensatory mechanisms can provide the basis for a
remarkable reorganisation and recovery.
Serial
assessment of psychological status by a clinical psychologist is helpful,
as is occupational therapy.
