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| COMMENTARY ON PEARLS FROM PAST |
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| Year : 2023 | Volume
: 71
| Issue : 1 | Page : 5-8 |
Commentary on Paper by S. Kalyanaraman and B Ramamurthi Primary Brain Stem Injury, Neurology India 17, 68-72, 1969
Prakash N Tandon
National Brain Research Centre, Manesar, Gurugram, Haryana, India
| Date of Submission | 04-Feb-2023 |
| Date of Decision | 04-Feb-2023 |
| Date of Acceptance | 04-Feb-2023 |
| Date of Web Publication | 24-Feb-2023 |
Correspondence Address:
Prakash N Tandon
National Brain Research Centre, Nainwal Mode, Manesar, Gurugram - 122 051, Haryana
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.370487
How to cite this article:
Tandon PN. Commentary on Paper by S. Kalyanaraman and B Ramamurthi Primary Brain Stem Injury, Neurology India 17, 68-72, 1969. Neurol India 2023;71:5-8 |
“In many general surgical works today the diagnosis of primary brain stem injury amounts to pronouncement of death sentence” (Kalyanaraman and Ramamurthi 1969)
It is interesting that around the same time as the above statement on ominous saying in some centers in Delhi acquired a similar predicament, “Yeh to brain stem ho gaya ab iska kuch nahi ho sakta” (He has become brain stem, now nothing can be done about it). This obviously led to “therapeutic nihilism” virtually lack of efforts to save the life of a severe head injured patient.
Kalyanaraman and Ramamurthi in their paper on primary brain stem injury, no doubt a serious condition, attempt to provide evidence to the contrary.[1] Utilization of clinical criteria proposed by Busch, they diagnosed 42 cases of primary brain stem injury among 1100 patients of head injury admitted to their head injury unit, first of its kind in India. They reported survival of 12 out of these 42 patients (28.6%)—three returned to work, and six were ambulant but not back to work. Two were bed ridden 1.5–2 years after injury.[2] No doubt a far better outcome than which was “generally” implied by the above statement (for details of brain stem hemorrhage—primary or secondary—see Tandon 1964, Tandon and Kristiansen 1965).[3],[4]
They provided a detailed analysis of these patients and advocated a certain therapeutic regime. Autopsy on 12 cases confirmed the clinical/fatal diagnosis, thus reiterating the correctness of the clinical criteria utilized for the study. Prognostic criteria were outlined.
While several reports for many years after this publication mentioned the paucity of such studies, at least the pathologists had described brain stem damage due to head injury as early as the end of nineteenth century.[5],[6] For historical details, see Tandon 1964, Tomlinson 1970, and Poppen 1952.[3],[7],[8] It should be mentioned that brain stem injury in both clinically and pathologically diagnosed cases was divided into 1) primary and 2) secondary. The primary injury is the direct result of the impact of trauma, while secondary injury is usually the result of the raised intracranial pressure. Secondary injury is usually due to raised intracranial pressure secondary to supratentorial lesions like hematomas and cerebral edema, resulting in tentorial herniation and its effect on the brainstem compression.[9]
As a matter of fact, clinical signs of the brain stem dysfunction often occur without structural damage (Tandon 1967).[10A, B] In an earlier publication, we had stated “The loss of consciousness associated transient loss of neurological functions seen in patients with concussion are obviously due to primary disturbance of brain stem function. Only rarely do the forces of trauma produce gross brain stem damage and hemorrhage due to bruising and mechanical strain (Tandon and Kristiansen 1965).[4] The coma in those fully recovering must have been due to primary distortion of brainstem and its functional disturbance without the irreversible ischemia or hemorrhage, which may occur subsequently. Furthermore, “Severe head injuries often lead to a chain of reactions which result in transtentorial herniation of medial temporal lobe resulting in compression of the brain stem and its vascular supply. This results in secondary brain stem dysfunction. Crompton (1971) described the microscopic pathology of primary brain stem injury among 106 patients dying soon after acute head trauma (See later under pathology.[11] He quoted the earlier such studies by Courville (1945) and Oppenheimer (1968).[12],[13]
Incidence: Prior to modern imaging techniques, the diagnosis of brain stem injury in non-fatal head injured patients was based on clinical signs. With minor variations, these included impairment of consciousness, decerebrate rigidity or generalized flaccidity, pupillary abnormalities, disturbance of ocular gaze, and autonomic dysfunction. We recorded that most of these clinical features could occur even in autopsy-proven cases of fatal head injury without any structural damage to the brainstem (Tandon 1964, Tandon and Kristiansen 1965).[3],[4] This has been confirmed after recent imaging studies. Kalyanaraman and Ramamurthi (1969) reported 42 cases of brain stem injury among 1100 cases of head injury patients admitted to their head injury unit in 18 months.[1] As late at 2007, Shukla et al. stated, “Several autopsy studies of head injury are available, but pathology of brain stem and hypothalamus injury are addressed in very few of them. Authors described the pathology of 47 such cases following a CT study of 1000 cases of head injury found 19 cases of primary and 48 cases of secondary brain stem injury.[14] Zuccarello et al. 1983 in study of 1000 cases of head injury reported 36 cases of primary brain stem hemorrhage.[15] Britt et al. (1980) found 41 cases of primary brain stem injury among 162 cases of head injury.[16] Gentry et al. (1989) stated that, “to our knowledge, the frequency of brain stem injury in patients with non-fatal head injury has not been previously determined because of very low sensitivity of CT in detecting these lesions.[17] It may be pointed out that the diagnosis of primary brain stem injury remains difficult even after the recent advances in imaging, Cooper et al. (1979), Zuccarello et al. (1983), Gentry et al. (1989), and Tsal et al. (1980).[16],[17],[18],[19] On the other hand, most reports on autopsy studies on fatal head injury patients rely on naked eye finding, not using detailed microscopic histological studies.[18] Kristiansen and Tandon 1960, Tandon 1964, Crompton 1971, Shukla 2007, and Tomlinson 1970 highlighted the need for microscopic examination to detect lesions in the brain stem, often not visualized by the naked eyes.[8],[11],[19],[20] Severe lesions may be present within the brainstem appear normal to the naked eyes. Credit for later goes to Hume Adams of Glasgow. Mitchell and Adams (1973) after detailed microscopic studies of over 100 fatal head injured patients made the following observation, “It is suggested that the so-called” primary brain stem injury does not exist in isolation but is only an aspect of diffuse brain damage.[21] They described the striking histological features as extreme rarefaction of tissue and presence of axonal retraction balls which are similar to the “Stritch” lesions characteristic of diffuse axonal injury. They repeated this observation in several other papers later on (Adams et al. 1977, 1982, Adams 1992).[22],[23],[24] This has been confirmed by Zuccarello et al. 1983. While there may be some truth in this statement of primary injury to brain stem, Britt et al. 1980, Crompton 1977, Wong 1993, and Crompton (1977) in autopsy study of 206 patients of dying soon after acute head injury reported that one-third (32) of them had primary brain stem injury.[11],[25]
According to Gentry et al. (1989), the frequency of brain stem injury in patients with fatal head injury has ranged from 2 to 100% depending on the length of patients survival and method of pathological analysis.[17] Clifton et al. (1981) reported 75% of patients who died within two days of trauma had evidence of serve brain stem injury, Crompton (1977) in a similar series of 206 patients reported a frequency of 87%, and Jellinger and Seitelberger in a series of 576 autopsy cases with slightly longer survival time noted 49.5% frequency.[11],[26],[27] Cooper et al. (1979) pointed out difficulty in detected brain stem lesions, even hemorrhage with CT scan and reported a false negative result of 10–12% in the literature. Zuccarello et al. (1983) also highlighted this difficulty. Tsai et al. (1980) following CT scan study of 1000 head trauma cases found 67 with brain stem injury (19 primary, 48 secondary).
Gentry et al. (1989) carried out MRI and CT studies on 70 acute and 17 chronic patients of HI and found brain stem lesions 36. They found MR images more sensitive than CT to detect more common non-hemorrhagic lesions which are missed by CT.
| » Pathogenesis | |  |
Primary brain stem injury is the result of the direct effect of the trauma which results in its distortion and displacement. This leads to shearing of the nerve fibers, manifested as axon retraction bulbs, with or without microglial stars Mitchell and Adams (1973), Tomlinson (1970), Courville (1945), Lindenberg and Freutag (1970), Gentry et al. (1989), and Crompton (1971).[28] At the same time, it may produce shearing of small blood vessels resulting in microhemorrhage, especially in the mid-brain and rostral pons (Shukla et al. 2007, Shanker & Mahadeven 2012).[29] The displacement of the brain stem may be responsible for contusion or tear along its lateral aspect caused by the rigid tentorial edge (Mohapatra and Kumar (2012).[30] The associated vascular injury can lead to ischemic necrosis and brain stem edema (Tomlinsons 1970). At times, the impact of the trauma is so severe as to result in complete transection of the brain stem. Britt et al. (1980) in services of 162 consecutive fatal cases of head were first described by Vogt et al. (1962).[31] The paucity of such lesions reported in large autopsy series of severe head injury is due to the sudden death of these patients at the site of injury. Hence, they fail to reach hospitals for neuropathological studies. They are subject of study by forensic pathologists. The precise pathogenesis of these severe lesions is not described, but obviously very high-velocity traffic accidents are no doubt responsible for these.
| » Pathology | | |
The pathology of primary brain stem injury varies from microscopic lesions like those of diffuse axonal injury, microscopic or macroscopic petechial hemorrhages, large hematomas, to contusion, tear, and transection mentioned above. While brain stem hemorrhage is more common in the secondary group of brain stem lesions, these are not uncommon in the primary injury especially in the lateral part of the mid-brain, the superior cerebellar peduncle, and rostral pons. These have been described in the hypothalamus but seldom in the distal pons and medulla. These may be single or multiple, small petechial or as large hematomas (Tandon 1964, Tomlinson 1970, Crompton 1971, Shukla et al. 2007).[32]
| » Clinical Features | | |
It is generally agreed that brain stem involvement in the head injured patients results in loss of consciousness, unilateral or bilateral, dilated, and non-reacting pupils, disturbance of muscle tone with decerebrate rigidity, disturbance of respiration, and autonomic functions. Kalyanaraman and Ramamurthi (1969) accepted the same as summarized by Busch (1963). In addition, we studied the vestibulo–ocular reflex to evaluate the brain stem pathology. It proved to be a sensitive investigation for diagnosis and prognosis of patients who clinically suspected to have brain stem involvement (Jadhav et al. 1971, Tandon et al. 1973).[32],[33] This was found to be equally if not more sensitive than the brain stems evoked response (BAER).[34]
It is important to emphasize that these symptoms and signs of brain stem injury do not imply irrevocable fatal outcome as once believed. Already in 1960s, we pointed out that these may be signs of brain stem dysfunction and not irreversible structural damage (Kristiansen and Tandon 1960). Furthermore, even some structural damage, including hemorrhage, does not result in fatal outcome. Thus in 1964, we pointed out that, “A similar clinical picture is, however, also seen, though less frequently, in both fatal and surviving cases without brain stem hemorrhage (Tandon 1964).
This observation is supported by the study reported by Kalyanaraman and Ramamurthi (1969). Following the availability of CT and MR imaging, there have been a number of studies establishing recovery following brain stem hemorrhage in patients with acute head injury (Cooper et al. 1979, Zuccarello et al. 1983, Tsai et al. 1980, Wong 1993, Johnson 1986, Bhutani et al. 1993). However, most of these authors commented on survival of such patients in vegetative state. In contrast, a study of 70 patients with CT established brain stem hemorrhage from our department revealed survival of 38, among whom 22 patients had good recovery, six were severely disabled or remained vegetative (Mahapatra and Kumar 2012). Useful survival has also been reported by Maciver et al. 1958, Cooper et al. 1979, Wong 1993, Kim et al. 1985, Bhatoe 1999, and Gyory 1985.[35],[36],[37],[38],[39]
| » Conclusion | | |
The paper by Kalyanaraman and Ramamurthi (1969) was as timely addition to the subject on which there were few authentic studies at that time. At the same time, it was an attempt to disprove the unfortunate prevailing impression about the futility of active management of such patients. Later studies mentioned above confirmed their optimistic views about the outcome. Attempts have been made in this commentary to provide a summary of the more recent studies on the subject.
| » Supplementary material | | |
| » References | | |
| 1. | Kalyanaraman S, Ramamurthi B. Primary brain stem injury. Neurol India 1969;17:68-72.,  |
| 2. | Busch EAV. Brain stem contusion: Differential diagnosis, therapy and prognosis. Clin Neurosci 1963;9:18-33. |
| 3. | Tandon PN. Brain stem harmorrhage in cramio-cerebrak trauma. Acta Neurol Scandinav 1964;40:375-85. |
| 4. | Tandon PN, Kristiansen K. Clinicaopathological observations on brain stem dys function in cram cerebral injuries. Excerpta Medica. International Congress Sense No. 11: Proceedings of IIIrd International Congress of Neurological Surgery, Copenhagen, 1965. p. 126-9. |
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| 23. | Adams JH, Gennarelli, TA, Graham DI. Brain Damage in non-missile head injury: Observations in man and non-human primates. In: Smith WT, Cavanagh JB, editors. Recent Advances in Neuropathology no 2. Edinburgh: Churchill Livingston; 1982. p. 165-90. |
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| 25. | Wong C-W. The MRI and Ct evidence of primary brain stem injury. Surg Neurol 1993;39:37-40. |
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| 30. | Mahapatra AK. Kumar R. Traumatic Brain Stem Haemorrhage in Textbook of Traumatic Brain Injury. New Delhi: Japyee Brothers Medical Publisher (P) Ltd; 2012. p. 284-9. |
| 31. | Alexis RJ, Jagdish S, Sukumar S, Pandit VR, Palnivel C, Antony MJ. Clinical Profile and Autopsy Findings in Fatal Head Injuries. J Emerg Trauma Shock 2018;11:205-10. [ PUBMED] [Full text] |
| 32. | Jadhav WR, Sinha A, Tandon PN, Kacker SK, Banerji AK. Cold caloric test in altered states of consciousness. Laryngoscope 1971;81:391-402. |
| 33. | Tandon PN, Bhatia R, Banerji AK. Vestibulo-ocular reflex and brain stem lesions. A clinico-pathological study. Neurol India 1973;21:193-9. |
| 34. | Mahapatra AK, Tandon PN. Brain stem auditory evoked response and vestibulo – ocular reflex in severe head injury patients. Acta Neurochir (Wein) 1987;87:40-5. |
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