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
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.
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.
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.
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.
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.
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.
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