Brainstem Hemorrhage Research Articles

Brainstem hemorrhages and increased intracranial pressure: From Duret to computed tomography

In the late nineteenth century, Henri Duret produced minute brainstem hemorrhage in dogs by rapidly increasing their intracranial pressure. Whether those hemorrhages were the same as those seen today associated with transtentorial herniation is not agreed upon, and the term Duret's hemorrhages is rarely used. Duret's report on his experiments is condensed here and the value of computed tomography for detecting brainstem hemorrhages is illustrated by a case report.

Classification of Computerized Tomography and Prognosis of Traumatic Primary Brain Stem Injury

Clinical signs, computerized tomography (CT), continuous monitoring of intracranial pressure (ICP), serial recording of auditory brain stem response (ABR), and autopsy were examined in 40 cases of primary brain stem injury (PBSI) which showed clinical symptoms of prolonged coma, abnormal motor responses (decorticate, decerebrate or flaccid), impaired oculocephalic and/or pupillary responses, and no evidence of focal mass lesions on initial CT scanned within 2 hours after the injury. The consciousness levels of the 40 cases of PBSI on admission were 5 or less by the Glasgow Coma Scale; 5 in 12 cases; 4 in 15 cases; 3 in 13 cases. CT findings of the brain stem region (mesencephalon, pons, and medulla oblongata) of PBSI were classified into 7 types: brain stem hemorrhage (Type I); IVth ventricle hemorrhage (Type II); subarachnoid hemorrhage in the basal cisterns (Type III); compressed basal cisterns (Type IV); pneumocephalus in the basal cisterns (Type V); combined abnormal findings in the brain stem regions (Type VI); no abnormal findings in the brain stem regions (Type VII). Those cases of PBSI with initial CT findings of Type I, Type II, Type III, Type V, and Type VI all died. On the other hand, 7 cases of PBSI (17.5%) demonstrating good recovery or moderate disability by the Glasgow Outcome Scale (6 months after injury) were of Type IV (mortality 66.7%) and Type VII (mortality 50%); 5 of these cases (71.5%) were children. It has become obvious that there are many types of CT findings in PBSI besides brain stem hemorrhage that continuous ICP monitoring is very important to protect against secondary brain damage caused by increased ICP and that serial ABR recording predicts the outcome of PBSI very well as it provides reliable information about the function of the brain stem.

Continuous vertical ocular flutter, asynchronous palatal myoclonus, and alpha coma

A patient is described who suffered a massive brainstem hemorrhage and survived in unreactive alpha coma for eight months. During this time, continuous vertical ocular oscillations were observed and recorded. The eyelids were open and followed the movements of the eyes. Palatal myoclonus was present, along with periodic facial synkinesias and 'ratchet-like' respirations, all of which followed independent rhythms. Review of the literature documented the uniqueness of this association and provided a framework for understanding the relationships among the various phenomena.

Electrocardiographic changes in cerebrovascular hemorrhage

The electrocardiographic abnormalities found in localized cerebrovascular hemorrhage which have been documented by computerized tomography (CT) scans are described. Frontal lobe hemorrhages are associated especially with the electrocardiographic abnormalities of QT prolongation and neurogenic T waves. Brain stem hemorrhage seems to be associated with noncardiogenic pulmonary edema, and sudden development of atrial fibrillation. It is proposed that the cause of ECG abnormalities in association with lesions in the vincinity of area 13 on the orbital surface of the frontal lobe, or around the circle of Willis, results from alterations in sympathetic and parasympathetic tone mediated by fibers from the orbito-frontal area to the heart via the stellate ganglia.

Pattern of cranio-intracranial injuries in fatal vehicular accidents in Delhi, 1966--76.

The present study was undertaken in the Department of Forensic Medicine of the AH India Institute of Medical Sciences, New Delhi, with the object of studying various aspects of cranio-intracranial injuries in roadside vehicular accident cases. Out of a total of 3227 medicolegal post-mortem examinations conducted, the number of accidental deaths was 2279 (70·62 per cent). Vehicular accidents (1132) comprised 49·76 per cent of the total fatal accidents and 35·5 per cent of the total post-mortems. The incidence of males involved in accidents was 71·74 per cent which was about five times more than females (15·01 per cent). Children below 12 years comprised 13·25 per cent of vehicular accident victims. The most common victim involved was the pedestrian comprising 50·7 per cent, followed by the motorcyclist (18·28 percent). The commonest age group involved in fatal vehicular accidents was between 21–40 years (521 cases, 46·01 per cent). Persons between the age group 11–20 years accounted for 13·69 per cent. Trucks were responsible for accidents in 28·09 per cent of cases, buses in 17·14 per cent and cars in 22·99 per cent; these have been found to be the most common types of vehicles causing fatal accidents. Most of the victims died on the spot (36·30 per cent). A total of 72·5 per cent of the victims died within 24 hours. All victims survived up to a maximum of only 2 weeks, except one case who survived 29 days and died of pyogenic meningitis. Head injuries were responsible for causing death in 71·99 per cent of cases. Chest injuries caused death in 6·18 per cent of cases and abdominal injuries proved fatal in 7·06 per cent of cases. Death by injury to other regions occurred in 15·54 per cent of cases. The incidence of cranio-intracranial injuries was highest in cyclists (78·93 per cent), followed by motorcyclists (72–46 per cent) and pedestrians (66·02 per cent). The number of car occupants involved in fatal accidents was 65·3 per cent. Fracture of the skull was observed in 79·87 per cent of cases; the most common bone involved was the temporal bone (58·67 per cent), followed by the occipital bone (57·75 per cent). Fractures of parietal and frontal bone were almost equal, being 50·38 per cent and 49·37 per cent respectively. The commonest variety of intracranial haemorrhage was subarachnoid haemorrhage (66·9 per cent), followed by subdural haemorrhage (58·2 per cent) and extradural haemorrhage (14·2 per cent). Extradural haemorrhage was least common (14·2 per cent). Intracerebral haemorrhage was found in 22·5 per cent of cases and brain stem haemorrhage in 10·81 per cent. The incidences of contusion and laceration of the brain were almost equal, being 23·6 per cent and 24·8 per cent respectively. Fracture of the ribs was the commonest chest injury, with contusion and laceration of the lung in 18·6 per cent of cases. Laceration of the liver was commonly found in abdominal injury in 17·2 per cent of cases. These findings have been compared with other authors. An attempt was also made in the present study to correlate the post-mortem findings and the survival time in relation to those victims who gave a history of consciousness after the accident and those where there was no history of consciousness. For convenience sake, the post-mortem lesions were divided in grades as 0, I, II, IIa, III and IIIa. The maximum number of fatal cases (46·2 per cent) belonged to grade III (fractured skull, intracranial haemorrhage and brain lesion) followed by grade II (35·1 per cent) (fracture skull and intracranial haemorrhage). No relationship was established between the post-mortem findings, the survival time and the state of consciousness or un-consciousness. The grade II and grade III lesions were common in both conscious and unconscious patients. The commonest complication observed in head injury cases was bronchopneumonia.

Traumatically Induced Brain Stem Hemorrhage and the Computerized Tomographic Scan

Abstract The computerized tomographic (CT) scan has revolutionized the management of cerebral trauma. Nevertheless, visualization of traumatically induced lesions of the brain stem by the CT scanner remains difficult. Seven patients with autopsy or CT evidence of brain stem hemorrhage were identified over a 1-year period. In six of these patients, brain stem hemorrhage could be defined by CT scan. As part of a prospective study of CT changes after head injury, we performed serial CT scans on six of the seven patients. Clinical experience shows that timing is important for identification of these lesions and that inability to visualize brain stem hematomas may occur because of the development of hematomas after CT scanning, evolution of hemorrhagic lesions that makes them isodense with the surrounding brain stem, patient movement, and technical factors such as the partial volume effect. Experimental injection of fresh blood into the pons and midbrain of cadavers shows that lesions as small as 0.1 ml in volume may be visualized by ex vivo thin section CT scanning techniques. However, the character and anatomical configuration of the hemorrhage may be as important in determining CT visualization as is the volume of the hemorrhage. For example, a hematoma displacing the brain parenchyma was visualized, but a similar-sized small hemorrhage that had diffused through the brain stem tissues was not. Although many of the experimentally placed lesions extended over a rostral-caudal length of 15 mm or more in the brain stem, no lesion was seen on more than three thin section scans. This is explained by the presence of lesions that, although extensive in a rostral-caudal direction, had relatively small cross sectional areas available for identification by the CT scanner. The small size of traumatic lesions of the brain stem and their proximity to bony structures at the base of the skull are not insurmountable obstacles to visualization of brain stem hemorrhages. Serial scanning and the application of thin section computed tomography will lead to identification of most of these lesions.

Traumatically induced brain stem hemorrhage and the computerized tomographic scan

Traumatically induced brain stem hemorrhage and the computerized tomographic scan

Otoneurological Findings in Patients with Brain Stem Lesions

We report about the otoneurological findings in 31 patients with brain stem lesions and comparison of the results between the standard auditory examinations and the vestibular examinations. The 31 patients were diagnosed as follows; acoustic tumors, 14; meningiomas in cerebellopontine angle, 3; trigeminal neurinoma in CPA; 1; cholesteatoma in CPA, 1; fibroblastoma in CPA, 1; brain stem glioma, 8; brain stem hemorrhage, 3. The abnormal findings of the auditory brain stem responses in these patients were divided into two patterns. In one pattern, the latency of the fifth wave was delayed. In the other, the fifth wave was not apparent. The vestibular findings suggested brain stem disturbance in patients in whom the auditory brain stem responses were also abnormal.

Cerebellar hemorrhage in adults. Diagnosis by computerized tomography.

A series of 10 adult patients with cerebellar hemorrhage diagnosed by computerized tomography (CT) is described. Hypertension was the most common etiological factor, accounting for 70% of the cases. The clinical presentation appeared to fall into two basic groups. The first group (60% of the cases) ran a progressive course with early brain-stem compression. The second group had a benign course with findings of focal cerebellar dysfunction. The CT findings reflected the two clinical categories. The scans of Group 1 patients revealed a lorge hematoma (greater to or equal to 3cm) and substantial ventricular dilatation. In contrast, scans of Group 2 patients demonstrated a small hematoma (less than 3 cm) without ventricular dilatation. Use of CT scanning allowed the accurate diffferentiation of cerebellar hemorrhage from primary brain-stem and intraventricular hemorrhage. The findings of the CT investigations proved very helpful in defining appropriate therapy.

Progressive ataxia in Charolais cattle.

Progressive ataxia in pure-bred Charolais cattle first was seen in England [ l ] and has since been recognized in Canada, New Zealand [3] and France [2]. Neurologic disturbances usually begin between 1 and 2 years old but have been seen as early as 6 months. There is progressive incoordination. Inability to rise develops over a period of months; urinating in an uneven flow is an early abnormality in females [3]. Vision, alertness, appetite and appendicular muscle tone and mass remain normal. In sections stained with hematoxylin and eosin (HE), myelinated parts of the optic nerves, brain and spinal cord have ill-defined foci of fine filaments separated by a pale-pink ground substance (fig. 1, 2). The foci or plaques tend to be more numerous in specific anatomic areas [l]. Normal axons are within these foci of disordered myelin (fig. 3). Oligodendroglia adjacent to the plaques may be hypertrophied with a round vesicular nucleus, dense peripheral chromatin and granular cytoplasm, which gives them an epithelioid appearance (fig. 2). Ultrastructurally , the lesion of the myelin sheath is adjacent to nodes of Ranvier and consists of hypertrophied and hyperplastic oligodendrocytic projections from which arise many small processes. There also are incomplete myelin lamellae and paranodal myelin figures [l]. These changes reflect a defect of unknown cause in oligodendroglia. Progressive ataxia has been seen in twin purebred Charolais heifers born in Oklahoma. Twin 1 at 6 months had posterior incoordination; by 8 months this had progressed to walking with a stilted gait and legs spread apart. At rest the rear legs were held forward. At 1 year old she could not rise on her hind legs without assistance. She was killed and necropsied. Peculiarities in urination were not recorded. No gross lesions were seen at necropsy except a torn round ligament and subluxation of the right femoral head. At 8 months twin 2 had posterior incoordination. She died when she was 2 years old. During the last weeks she could rise only with assistance; bloat had to be relieved several times. Two weeks before she died she had a heifer calf which remains unaffected at the age of 8 months. A limited postmortem examination showed subdural hemorrhage of the ventral brain stem and anterior cervical spinal cord. Microscopic changes of the central nervous systems were similar to those in previous reports and have been verified [2]. Moderate perivascular infiltrates of

Experimental Primary Fatal Head Injury Caused by Linear Acceleration—Biomechanics and Pathogenesis

The present experiment was undertaken to clarify the pathogenesis of primary fatal head injury due to impact and further to obtain a severity index denoting the relationship between the magnitude of impact and the severity of head injury in animals with experimental blunt head injuries caused by simplified impact upon the cranium. The experiment was conducted on Ketalar-anesthesized rhesus monkeys. Impact was imparted to the animals by means of a 12 in. HYGE impact tester. Before and after the impact the animals were subjected to a series of examinations at intervals, including respiration, ECG, blood pressure, cerebral circulation, partial pressure of blood gases, acid-base equilibrium and EEG. Pathological examination, measurements of lactic acid and monoamine contents in various portions of the brain were also made. An impact upon the head, at an acceleration in the horizontal antero-posterior direction of 1000-1500 G and a duration of 3-4 msec, proved fatal invariably in animals weighing more than 8 kg (body weight×effective acceleration above 30 kg). In dead animals, primary injury consisting of narrowing of lumen and stoppage of blood flow in perforating arteries of the brain-stem and small hemorrhages in the same areas was noted. It was demonstrated that these changes give rise to central dysregulation of the circulatory (including heart) and respiratory systems which in turn acts on cerebral circulation and metabolism. This fact not only proves the existence of a primary fatal head injury and further clarifies its mechanism of development but also suggests the possibility of grading the severity of head injury by simplified impact and also by expressing the relationship between the magnitude of impact and the severity of brain damage as a severity index.

Massive cerebral infarction with severe brain swelling: a clinicopathological study.

All cases of acute supratentorial cerebral infarction which came to postmortem examination over the past 10 years at the Philadelphia General Hospital were reviewed. Of a total of 353 such cases, 45 showed severe brain swelling. Seventy-eight percent of these 45 patients died within seven days of the acute infarction. The rapidly fatal outcome appeared to be directly related to the acute brain swelling with transtentorial herniation and brain-stem edema or hemorrhage. In those patients who survived longer than one week following onset of the ictus (22%), clinical and anatomic findings suggested that increased intracranial pressure probably did not develop until later in the course of the illness. A second massive infarct was probably superimposed upon an earlier one and produced the acute brain swelling noted at the time of postmortem examination. Complicating visceral diseases were more common in this group and seemed to contribute to death in the majority of these patients. Although it has been established that a large cerebral infarct may produce sufficient brain swelling and simulate an acutely expanding lesion, this is not widely recognized as playing an important part in determining the patient's clinical outcome. The role of increased intracranial pressure resulting from acute brain swelling should not be overlooked in the management of patients with severe strokes.

Rubral Tremors Associated with an Inferior Olivary Lesion that Developed after a Brainstem Hemorrhage

Rubral Tremors Associated with an Inferior Olivary Lesion that Developed after a Brainstem Hemorrhage

Secondary brain stem hemorrhages. Predisposing and modifying factors.

TRANSTENTORIAL herniation, a recognized complication of expanding supratentorial lesions, is often heralded clinically by impairment of consciousness and other changes in vital signs, culminating frequently in decerebration and death.1-4These latter clinical events have been ascribed to secondary hemorrhagic extravasations in the midbrain and pontine tegmentum within the distribution of the mesencephalic perforating arteries (Fig 1 and 2). The purposes of this analysis of a large autopsy population are: first, to discern which of the preceding supratentorial lesions may preferentially lead to secondary brain stem hemorrhage (2° BSH), and secondly, to assess in retrospect the influence of other factors, such as age and sex, upon the frequency of this secondary lesion. Patient Material The data presented in this paper derive from 199 cases of 2° BSH which were extracted from the 7,110 consecutive, completely autopsied cases in the records of the Institute of Pathology, Kings County Hospital Center,

Israel society for electroencephalography and neurophysiology: Secretary: Dr. S. Lavy

Ocular motility has been studied in comatose patients by means of caloric stimulation of the labyrinth. The investigation is carried out by injecting 20 ml of water at 20°C or 41°C into the external auditory meatus.The various responses observed in cases of lesions of the central and peripheral oculogyric pathways are discussed, clinical data being correlated with anatomical findings.When no severe lesion is present in the vestibulo-oculogyric pathways upon injecting cold water, a slow deviation of the eyes towards the stimulated labyrinth is elicited; when warm water is used, the deviation is toward the contralateral side. Only the slow phase is obtained, because in a comatose patient, the rapid nystagmic response is abolished.The various types of response and the underlying clinical and pathological findings have been considered. 1.(1) A positive response on both sides indicates non-involvement of the lower portion of the ocular motor tract and usually excludes serious brainstem lesions.2.(2) An absence of response to stimulation on either side (‘frozen eyes’) indicates a severe bilateral lesion of the vestibulo-oculogyric tract in the brainstem.3.(3) No horizontal response but vertical nystagmus only is found particularly with brainstem haemorrhages.4.(4) Lack of response towards one side, either with cold water (homolateral) or warm water (contralateral) indicates pontine paralysis of lateral gaze.5.(5) Downward movement of both eyes on labyrinthine stimulation reflects involvement of the superior colliculus on the side toward which the eyes are elevated. It may be bilateral, in which case the eyes move always below the palpebral fissure.6.(6) Asymmetrical responses6.1.(i) Total or partially limited abduction is common with paralysis of the sixth nerve.6.2.(ii) Total or partially limited adduction indicates paralysis of the third nerve or else an anterior internuclear ophthalmoplegia.6.3.(iii) Oblique deviation of one eye with respect to the other. Here it is observed that the reflex movements of labyrinthine origin are oblique; there is also a lowering or elevation of the eye on the side of the lesion on adduction owing to the affection of the 3rd or 4th nerve respectively.6.4.(iv) Pure oblique deviations correspond with lesions which affect the nuclei or trunks of the oculo-rotatory nerves.6.5.(v) Alterations of the vestibulo-oculogyric tract together with a Horner syndrome indicate the lesion-bearing side. In the conscious patient the vertical deviation may correspond with two pairs of muscles, sometimes with some degree of concomitance: (a) inferior rectus of one eye and inferior oblique of the other; (b) superior rectus of one eye and superior oblique of the other. These same patterns are elicitable in the comatose state by studying reflex motility.A study of ocular motility in comatose patients may provide the topographical diagnosis of the lesion with considerable accuracy.

Evaluation of the role of neurosurgical procedures in the pathogenesis of secondary brain-stem haemorrhages.

Evaluation of the role of neurosurgical procedures in the pathogenesis of secondary brain-stem haemorrhages.

The study of ocular motility in the comatose patient

Ocular motility has been studied in comatose patients by means of caloric stimulation of the labyrinth. The investigation is carried out by injecting 20 ml of water at 20°C or 41°C into the external auditory meatus. The various responses observed in cases of lesions of the central and peripheral oculogyric pathways are discussed, clinical data being correlated with anatomical findings. When no severe lesion is present in the vestibulo-oculogyric pathways upon injecting cold water, a slow deviation of the eyes towards the stimulated labyrinth is elicited; when warm water is used, the deviation is toward the contralateral side. Only the slow phase is obtained, because in a comatose patient, the rapid nystagmic response is abolished. The various types of response and the underlying clinical and pathological findings have been considered. 1. (1) A positive response on both sides indicates non-involvement of the lower portion of the ocular motor tract and usually excludes serious brainstem lesions. 2. (2) An absence of response to stimulation on either side (‘frozen eyes’) indicates a severe bilateral lesion of the vestibulo-oculogyric tract in the brainstem. 3. (3) No horizontal response but vertical nystagmus only is found particularly with brainstem haemorrhages. 4. (4) Lack of response towards one side, either with cold water (homolateral) or warm water (contralateral) indicates pontine paralysis of lateral gaze. 5. (5) Downward movement of both eyes on labyrinthine stimulation reflects involvement of the superior colliculus on the side toward which the eyes are elevated. It may be bilateral, in which case the eyes move always below the palpebral fissure. 6. (6) Asymmetrical responses 6.1. (i) Total or partially limited abduction is common with paralysis of the sixth nerve. 6.2. (ii) Total or partially limited adduction indicates paralysis of the third nerve or else an anterior internuclear ophthalmoplegia. 6.3. (iii) Oblique deviation of one eye with respect to the other. Here it is observed that the reflex movements of labyrinthine origin are oblique; there is also a lowering or elevation of the eye on the side of the lesion on adduction owing to the affection of the 3rd or 4th nerve respectively. 6.4. (iv) Pure oblique deviations correspond with lesions which affect the nuclei or trunks of the oculo-rotatory nerves. 6.5. (v) Alterations of the vestibulo-oculogyric tract together with a Horner syndrome indicate the lesion-bearing side. In the conscious patient the vertical deviation may correspond with two pairs of muscles, sometimes with some degree of concomitance: (a) inferior rectus of one eye and inferior oblique of the other; (b) superior rectus of one eye and superior oblique of the other. These same patterns are elicitable in the comatose state by studying reflex motility. A study of ocular motility in comatose patients may provide the topographical diagnosis of the lesion with considerable accuracy.

Brain stem hemorrhages secondary to supratentorial space-taking lesions.

Journal Article Brain Stem Hemorrhages Secondary to Supratentorial Space-Taking Lesions Get access James L. Poppen, M.D., James L. Poppen, M.D. Boston, Mass. *From The Department of Neurosurgery Search for other works by this author on: Oxford Academic PubMed Google Scholar John F. Kendrick, Jr., M.D., John F. Kendrick, Jr., M.D. Boston, Mass. †Fellow in Neurosurgery, The Labey Clinic, Boston, Mass. Search for other works by this author on: Oxford Academic PubMed Google Scholar S. F. Hicks, M.D. S. F. Hicks, M.D. Boston, Mass. ‡The photographs and description of the pathologic lesions in the text were provided by Samuel F. Hicks, M.D., Department of Pathology, New England Deaconess Hospital, Boston, Mass. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Neuropathology & Experimental Neurology, Volume 11, Issue 3, July 1952, Pages 267–279, https://doi.org/10.1097/00005072-195207000-00004 Published: 01 July 1952