K. E. Richard

Primary brain stem lesions caused by closed head injuries

Traumatic lesions of the brain stem are of two types: primary, which are considered to be caused at the moment of impact, and secondary, associated with supratentorial mass lesion. Of the 239 patients with a serious head injury who showed a severe disturbance of consciousness upon admisision and who had CT scan carried out immediately, 21 cases were considered to have a primary brain stem lesion with initial CT scan. A primary brain stem lesion was found in 21 of 239 (8.8%) of patients with serious head injury. Their injuries were caused primarily by traffic accidents. Sixteen of the 21 cases showed not only brain stem lesions but also other brain injuries such as cerebral contusion of the white and gray matter, callosal injury, intraventricular hemorrhage, and subarachnoid hemorrhage, which are considered to be caused by a diffuse shearing injury. Five cases who showed a single injury to the brain stem with no other brain lesions were considered to have a pure brain stem lesion. Primary brain stem lesions were observed on the dorsal side of the midbrain, where they can be differentiated from secondary brain stem lesions. These lesions are considered to result from the shearing mechanism in and around the brain stem very close to the tentorial edge, or to an injury of the lower brain stem by hyperextension of the cervical vertebrae. The prognosis of patients with a primary brain stem lesion was usually unfavorable, except in those with a single brain stem lesion.

Rehabilitation After Severe Head Injury

123 survivors of severely head injured patients presenting with coma grade III show a decreasing mean duration of coma with increasing age. The numbers and frequency of good recovery decrease, whereas poor recovery increases with age. Increase of the duration of coma grade III produces an increase of the mean latency and time of recovery and of the frequency of poor recovery, regardless of the age of the patients. Increasing age does not increase the mean latency and time of recovery systematically. The important conclusion of this analysis is, that the clinical feature of coma grade III, corresponding to GCS score of 4 and RLS of 6 and 7, indicates a different kind of brain damage at various age groups. It represents a lesser degree of brain damage for younger patients under 20, than for those over 20. In our opinion our observations do not demonstrate a better capacity of recovery of the young patients: but the young patients show a more severe clinical picture than the older patients do, if only the clinical syndrome of coma grade III with extensor rigidity, is considered as a yardstick for comparison.

Multiple injuries: coma and fractures of the extremities.

Between 1974 and 1985 195 patients with cranio-cerebral injuries and limb injuries were treated (Fig. i). The total mortality in patients with pure limb injuries or in combination with facial and skull injuries, with a clouding of consciousness was 7 %, in Coma I 13 %, in Coma II 48% and in Coma III 68 %. The mortality in Coma IV was I00 %, so no further discussion about this is possible (i). Additional facial and skull injuries did not raise the mortality significantly. Any attempt to distinguish the two groups is therefore considered unnecessary.

Humoral immunodeficiency syndrome in patients with severe head injury

SummaryTwenty patients with severe head injury were analysed as to whether they developed a humoral immunodeficiency syndrome. In spite of the fact that 75% developed pyogenic complications all patients showed a polyclonal humoral activation of their immune system with an increase in IgG, IgA, IgM and the complement factors.Four patients died from cerebral complications partly associated with infections. Because our patients did not develop a humoral immune defect and because there is no proof so far of a cellular defect, we think that the cause of respiratory infections is a pulmonary disturbance primarily caused by hypothalamic factors, whose release is stimulated by traumatically induced cerebral lesions.

Criteria for the Diagnosis of Brain Death

Since the first observation of the syndrome of “coma depasse” by MOLLARET and GOULON in 1959, 26 years ago, a second set of criteria for the diagnosis of brain death bas been presented in recent years, especially in Great Britain (SMITH 1979), in the USA (WALKER 1981, LYNN 1981), by the Bundesarztekammer (BAK) in Germany (WOLFF and KUHLENDAHL 1982), and in Switzerland (CHIOLERO et al. 1983).

Intracranial pressure: A reliable criterion of brain death?

Our question is how often and on what preconditions an ICP increase above the level of the systolic blood pressure Can be observed during the development of the brain death syndrome. In 21 patients we were able to record the ICP continuously; in 16 patients the epidural pressure (EDP) and in five patients the ventricular fluid pressure (VFP) during the development of a secondary brain death syndrome.

Acute hydrocephalus in infectious spinal disorder

Two patients with infectious spinal disorders and increased intracranial pressure are described. One patient with spinal empyema lapsed into coma but improved after external ventricular drainage to relieve increased intracranial pressure. The second patient, who had a severe wound infection after repeated operative stabilization of a cervical spine fracture, developed increased intracranial pressure and subsequent hydrocephalus 6 months after the trauma. The pathogenesis of hydrocephalus in infectious spinal disorder is discussed.

Coma and spinal injury

The 5 patients with cervical spine injuries were all in coma grade II, III or IV. Twelve of the remaining 15 had dorsal injuries; three other patients had injuries in the lumbar region. The most injured segment was D 12 and L i, as observed by other authors (2). There was a fairly even distribution of the 15 cases with dorsal and lumbar injuries between clouding of consciousness and comas grade I, II and III, with one case in coma grade IV. Three out of the 5 patients with severe cervical injuries died (that is, about 2/3), as against 1/3 of those with severe dorsal and lumbar damage. The mortality is considerably higher than for simple spinal injuries.

Significance of intracranial pressure for the outcome of patients with multiple injuries

On the day of trauma the mean intracranial pressure (ICPx) was not elevated. However, pressure peaks up to 50 mm Hg were recorded in 5% of the patients. By contrast, the mean ICP had increased in 21% of the patients with a fatal outcome. It is noticeable that two thirds of these patients were in coma IV with fixed pupils. On the first day after trauma the number of patients with normal ICP-values decreased significantly to 80 and 72%, respectively. In 12% of the survivors pressure peaks above 50 mm Hg occurred. This trend continued until the fifth post-traumatic day. After that, the percentage of the injured patients with normal ICP-values increased again.

Multiple injuries: Coma and abdominal injury

As expected, the 33 % mortality rate amongst patients with pelvic injuries was lower than the 76 % mortality rate amongst patients with injuries of the parenchymal abdominal organs (Figure i, 2). Out of a total of 9 patients with only abdominal injuries, neither of the 2 clouded, 3 of the 5 coma grade II patients and both the coma grade IV patients died. Of the i0 patients with facial injuries and/or injuries to limbs, as well as abdominal injuries, all 3 clouded or coma grade I patients survived. 3 out of 4 coma grade II and III patients and all 3 coma grade IV patients died. Just 1 clouded and 1 coma grade II patient survived out of 13 patients with combined abdominal-thoracic injuries. The remaining ii died, regardless of the degree of coma. In cases of additional injury to limbs and/or facial injuries 13 out of 14 patients also died, regardless of the degree of coma and only 1 clouded patient survived. Of a total of 19 coma grade IV patients, none survived so that they, as well as the only surviving clear patient, are excluded from further discussion.