PTS

Post-traumatic Syndrome is one of the most controversial topics in the field of head trauma. The controversy starts right from its terminological imprecision. There is no consensus of opinion in even what constitutes Post-Traumatic Syndrome. Synonyms include post concussion syndrome, post head injury syndrome and so on. Considerable literature exists regarding the management of moderate and severe head injuries. Literature on minor head injuries is relatively recent. Normal imaging studies reinforce the belief that these injuries do not produce structural brain damage.

A national survey of 397 family physicians, neurologists, neurosurgeons and orthopaedic surgeons (those primarily treating PTS) was done in June 1992 in the USA. Only a minority believed that the PTS was clearly defined. Many believed that psychogenic factors and litigation were responsible. Most believed that recovery occurred in 3-6 months. Many physicians ordered tests to rule out pathology while a minority did so to reassure patients or because of litigation concerns. Only a minority believed that effective treatment was available.

A large number of conventional and unconventional treatments were recommended. It may therefore not be surprising to find that this article also will raise questions rather than give clear-cut answers.

PTS does not appear to be uncommon in the developed countries. Reliable, scientifically accurate, statistically sound data is not available in India, with regards to the incidence and prevalence of the PTS. It is the impression of this author, based on 22 years of personal experience in managing a large number of minor head injuries, that the incidence is distinctly less. Other experienced neurosurgeons concur with this observation. The fact that litigation is less prevalent in India may partly account for this.

This term is loosely applied to combination of a wide variety of sequelae, which may follow minor head trauma. These include a group of syndromes for which there is no apparent pathological basis. The “ post concussional syndrome “ often encompasses a symptom complex, which includes transient dizziness, tinnitus, irritability, lack of concentration, easy fatiguability, and hypersensitivity to light and noise.

A combination of one or more of the following could be considered as forming part of the PTS.

· Headache

· Dizziness

· Vertigo

· Tinnitus

· Hearing loss

· Light and noise sensitivity

· Diminished taste and smell

· Irritability

· Anxiety

· Depression

· Personality change

· Fatigue

· Sleep disturbance

· Decreased libido

· Decreased appetite

· Memory Dysfunction

· Impaired concentration and attention

· Slowing of Reaction time

· Slowing of information processing speed

· Dystonia, Seizures

· Tremors

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.