Primary Brainstem Injury Research Articles

TRAUMATIC BRAINSTEM INJURY DUE TO BLUNT FORCE TRAUMA: AN AUTOPSY CASE REPORT

Trauma is the leading cause of morbidity and mortality in patients under 35-years of age and the sixth leading cause of death worldwide, but primary traumatic brainstem injury after blunt force trauma to the head is a rare event. A forensic autopsy was performed on a 35 years old female who was found dead in an apartment building with both her hands and feet tied together and mouth closed with duct tape. External examination showed the victim suffered from blunt force trauma to the head, face, both arms and legs. Internal examination of the body showed hematomas on the scalp, temporal muscles and deep neck muscles and organs, subarachnoid, intraventricular and brainstem haemorrhage and contusion, along with signs of asphyxiation. Trauma to the occipital region of the head not only can cause traumatic brain injury but can also cause trauma to the brainstem as a result from acute hyperflexion of the neck. Haemorrhages and contusions of the brainstem can lead to changes in the respiratory system, depending on the location of the lesions. Cause of death was concluded to be force trauma to the occipital region causing primary brainstem injury with the mechanism of death of asphyxia.

Metabonomics Analysis of Brain Stem Tissue in Rats with Primary Brain Stem Injury Caused Death.

To explore the potential biomarkers for the diagnosis of primary brain stem injury (PBSI) by using metabonomics method to observe the changes of metabolites in rats with PBSI caused death. PBSI, non-brain stem brain injury and decapitation rat models were established, and metabolic maps of brain stem were obtained by LC-MS metabonomics method and annotated to the HMDB database. Partial least square-discriminant analysis (PLS-DA) and random forest methods were used to screen potential biomarkers associated with PBSI diagnosis. Eighty-six potential metabolic markers associated with PBSI were screened by PLS-DA. They were modeled and predicted by random forest algorithm with an accuracy rate of 83.3%. The 818 metabolic markers annotated to HMDB database were used for random forest modeling and prediction, and the accuracy rate was 88.9%. According to the importance in the identification of cause of death, the most important metabolic markers that were significantly up-regulated in PBSI group were HMDB0038126 (genipinic acid, GA), HMDB0013272 (N-lauroylglycine), HMDB0005199 [(R)-salsolinol] and HMDB0013645 (N,N-dimethylsphingosine). GA, N-lauroylglycine, (R)-salsolinol and N,N-dimethylsphingosine are expected to be important metabolite indicators in the diagnosis of PBSI caused death, thus providing clues for forensic medicine practice.

Commentary on Paper by S. Kalyanaraman and B Ramamurthi Primary Brain Stem Injury, Neurology India 17, 68-72, 1969.

Commentary on Paper by S. Kalyanaraman and B Ramamurthi Primary Brain Stem Injury, Neurology India 17, 68-72, 1969.

COVID-19: Coronavirus replication, pathogenesis, and therapeutic strategies.

The frequency, distribution, and appearance of corpus callosum injuries were evaluated with MR and CT in a prospective study of 78 patients with acute (n = 63) and chronic (n = 15) head injuries. Traumatic lesions of the corpus callosum were detected in 47% of patients. MR was significantly (p less than .001) more sensitive than CT in the detection of callosal injuries. MR and CT visualized 100% and 27%, respectively, of the traumatic callosal lesions that were detected in the study population. The majority of lesions were located in the splenium but a few were also found in the body and genu. Patients with callosal injuries had a significantly higher incidence of primary brainstem injury (p less than .02) as well as a greater number of subcortical gray-matter (p less than .05) and diffuse axonal "shear" (p less than .001) lesions. In addition, patients with callosal injuries had a significantly higher incidence of traumatic lesions of the septum pellucidum (p less than .007) and fornix (p less than .001). Intraventricular hemorrhage occurred significantly more often (p less than .002) in patients with callosal injuries, especially if traumatic lesions of the fornix or septum pellucidum were also present. Patients with callosal injuries had significantly lower initial Glasgow Coma Scale scores (mean, 6.6) than those without injuries (mean, 10.7) (p less than .001). Injury to the corpus callosum occurs much more often with nonfatal head injuries than had been believed previously.

Identification of separation phenomenon during brain death determination of potential organ donor and analysis of relative factors

Background: With analyzing the incongruent phenomenon of electrical active and cerebral blood flow in brain death determination and screening the related factors, offer correct explanations and countermeasure to ensure the successful implementation of donation after brain death.Methods: Relevant clinical data of potential brain death organ donors were prospectively collected between June 2018 and May 2019. The related parameters of neurological examination, laboratory examination and neuroimaging examination during the period of brain death determination were dynamically recorded. Separation phenomenon was used as grouping factors to screen the factors related to separation phenomena through univariate and multivariate analysis.Results: According to the inclusion criteria, 127 patients were included in the study. Among 22 patients (17.3%) with incongruent phenomenon, 17 (77.3%) had electrical silence earlier than cerebral blood flow arrest, and 9 (22.7%) had cerebral blood flow arrest earlier than electrical silence. Univariate and multivariate analysis showed that age <14 years (OR=6.25, 95%CI 1.21-32.22, p=0.028), SBP≥140 mmHg (OR=7.43, 95%CI 1.62-33.99, p=0.010), primary brainstem injury (OR=15.89, 95%CI 3.04-82.93, p=0.006), spontaneous respiratory arrest time ≤72 hours (OR=11.96, 95%CI 1.59-89.78, p=0.009) and decompression craniotomy(unilateral or bilateral) (OR=16.28, 95%CI 2.25-117.73, p=0.001) were associated with separation phenomenon..Conclusions: Separation phenomenon is a common during the confirmation test of brain death determination in China, and should be correctly recognized. To adopt corresponding measures according to risk factors is useful for successful implementation of donation after brain death.

Endoscopically assisted supratentorial evacuation of infratentorial epidural hematomas crossing the transverse sinus

Abstract Objective Traumatic posterior fossa extradural hematoma (TPFEDH) is a serious complication of cranial injury and the orthodox technique for removal of TPFEDH encompasses a suboccipital craniectomy or craniotomy. However, in some cases, the TPFEDH might extend to the supratentorial space, thus appearing to be crossing the transverse sinus. Contrary to the standard way, a modified supratentorial transoccipital approach may be better suitable in the management of this subtype of TPFEDH. Methods The clinical data of 34 consecutive patients in which the TPFEDH was crossing the transverse sinus were prospectively assessed. We operated all the parents using the supratentorial transoccipital approach via supratentorial liner incision. The supratentorial extradural hematoma (EDH) was evacuated and the endoscope was used to fully evacuate the infratentorial compartment. Glasgow Coma Scale at discharge (dGCS) was documented and Glasgow Outcome Scale score (GOS) was measured at 3–15 months (mean = 5.4 months) follow-up subsequently. Results The average operation time was 44 min (30–60 min). The blood loss was so minimal that the intraoperative blood transfusion was unnecessary for all the patients. Complete hematoma removal was achieved on all the patients. The average dGCS and GOS were 14 and 4.9 respectively. One case suffered from primary brain stem injury whose GOS scored only 3 on follow up. There was no surgery related mortality at discharge and during the follow-up. Conclusion This is the first case series to demonstrate the removal of TPFEDH crossing the transverse sinus via the modified supratentorial transoccipital craniotomy. This approach was proven to be more effective in managing such cases.

Cortical Brain Changes in Patients With Locked-In Syndrome Experiencing Hallucinations and Delusions.

Previous evidence suggests that hallucinations and delusions may be detected in patients with the most severe forms of motor disability including locked-in syndrome (LIS). However, such phenomena are rarely described in LIS and their presence may be underestimated as a result of the severe communication impairment experienced by the patients. In this study, we retrospectively reviewed the clinical history and the neuroimaging data of a cohort of patients with LIS in order to recognize the presence of hallucinations and delusions and to correlate it with the pontine damage and the presence of any cortical volumetric changes. Ten patients with LIS were included (5 men and 5 women, mean age 50.1 ± 14.6). According to the presence of indicators of symptoms, these patients were categorized as hallucinators (n = 5) or non-hallucinators (n = 5). MRI images of patients were analyzed using Freesurfer 6.0 software to evaluate volume differences between the two groups. Hallucinators showed a selective cortical volume loss involving the fusiform (p = 0.001) and the parahippocampal (p = 0.0008) gyrus and the orbital part of the inferior frontal gyrus (p = 0.001) in the right hemisphere together with the lingual (p = 0.01) and the fusiform gyrus (p = 0.01) in the left hemisphere. Moreover, a volumetric decrease of bilateral anterior portions of the precuneus was recognized in the hallucinators (right p = 0.01; left p = 0.001) as compared to non-hallucinators. We suggested that the presence of hallucinations and delusions in some LIS patients could be accounted for by the combination of a damage of the corticopontocerebellar pathways with cortical changes following the primary brainstem injury. The above areas are embedded within cortico-cortical and cortico-subcortical loops involved in self-monitoring and have been related to the presence of hallucinations in other diseases. The two main limitations of our study are the small sample of included patients and the lack of a control group of healthy individuals. Further studies would be of help to expand this field of research in order to integrate existing theories about the mechanisms underlying the generation of hallucinations and delusions in neurological patients.

Incidence of critical illness-related corticosteroid insufficiency after severe traumatic brain injury and its correlations with prognosis

Objective To observe the incidence of critical illness-related corticosteroid insufficiency (CIRCI) after severe traumatic brain injury (sTBI) and investigate the relationship between CIRCI and prognosis. Methods This prospective cohort study enrolled 89 sTBI patients (68 males and 21 females; at age range of 15-80 years) hospitalized within 24 hours after sTBI from June 2014 to December 2015. The Glasgow coma scale (GCS) was ≤8 points. The causes of injury included extensive contusion of brain (44 cases), subdural hematoma (21 cases), epidural hematoma (11 cases), primary brain stem injury (8 cases) and diffuse axonal injury (5 cases). Adrenocorticotropic hormone (ACTH) stimulation tests were done within 36 hours after sTBI to identify CIRCI patients. The patients were divided into CIRCI group (50 cases) and non-CIRCI group (39 cases). Moreover, the patients were categorized into survival group (62 cases) and death group (27 cases) based on survival status. The GCS score, mechanical ventilation time, cerebral hernia, survival time and mortality within 28 days were observed in two groups. Results The incidence of CIRCI in sTBI patients was as high as 56% (50/89). Compared with the non-CIRCI group, the CIRCI group had lower GCS [(5.3±1.7)points vs. (6.1±1.4)points, P<0.05], and sTBI patients with CIRCI were mechanically ventilated for a longer period of time [(9.9±2.8)days vs. (7.5±1.6)days, P<0.05]. In comparison with non-CIRCI patients, the incidence of brain herniation in sTBI patients with CIRCI was higher (58% vs. 21%, P<0.01). The total fatality rate within 28 days was 30% (27/89). The survival time of CIRCI group was significantly shorter than that of non-CIRCI group (P<0.05). The fatality rate in the CIRCI group was significantly higher than that of the non-CIRCI group [40% (20/50) vs. 18% (7/39), P<0.05]. The incidence of CIRCI in death group was significantly higher than that of the survival group [74% (20/27) vs. 48% (30/62), P<0.05]. Conclusions The incidence of CIRCI in STBI patients is high. The sTBI patients with CIRCI has significantly higher incidence of brain hernia, longer mechanical ventilation time, higher 28-day mortality and shorter survival time compared with non-CIRCI patients. Key words: Brain injuries; Adrenocorticotropic hormone; Prognosis

A rabbit model of graded primary mechanical injury to brainstem

ObjectiveTo introduce a new animal model of graded mechanical primary brainstem injury (BSI). MethodsAltogether 45 rabbits were subjected to BSI by type II biological impact machine designed by the Third Military Medical University. The animals were divided into 4 experimental groups (n=10) and 1 control group (n=5) according to different magnitudes of impact pressure imposed on the occipital nodule: Group 1, 500-520 kPa; Group 2, 520540 kPa; Group 3, 540-560 kPa; Group 4, 560-580kPa and Group 5, 0kPa with 20kPa increase in each grade. The impact depth was a constant 0.5cm. After injury, the clinical symptoms and signs as well as pathological changes were observed. ResultsRabbits in Group 1 revealed mild physiological reaction of BSI. They had localized cerebral contusion with punctate hemorrhage and subarachnoid hemorrhage (SAH) was limited to the peripheral tissues at the impact area. In Group 2, obvious physiological reaction was observed. Local pathological lesions reached the superficial layer of brainstem tissues; focal hemorrhage and girdle-shaped SAH in basilar pon were observed under microscope. In Group 3, BSI was more severe with a long respiratory depression. Pathological lesions reached the inner portion of brainstem with massive hemorrhage and the whole brainstem was wrapped by subarachnoid hematoma. In Group 4, most rabbits died due to severe BSI. Pathological lesions deepened to the central brainstem with wide pathological change, rapture of the medulla oblongata central canal. Group 5 was the control group, with normal brainstem structure and no lesion observed. ConclusionThis model successfully simulates different levels of brainstem mechanical injury and clearly shows the subsequent pathological changes following injury. It takes two external parameters (impact pressure and depth) and has a similar injury mechanism to clinical accelerating BSI. Moreover it is reproducible and stable, thus being beneficial for exploring pathophysiological mechanism, diagnosis and forensic identification of various degrees of BSI.

Diagnostic Imaging of Primary Brainstem Injury Using Magnetic Resonance Imaging

Traumatic primary brain stem injury is brain stem injury caused by mechanical head trauma. Before the development of diagnostic imaging, a pathological examination has been the nearly only diagnostic method of primary brain stem injury. Because magnetic resonance imaging (MRI) has a high resolution and CT demonstrates much artifact around the brain stem, MRI became a powerful tool for investigating primary brain stem injury. There are some types of primary brain stem injury. The author herein reviews the recent clinical studies of MRI of primary brain stem injury. The importance of early MRI examination appears to be a consensus. Our study demonstrated that small superficial lesion may be detected only a few days after injury. The acute phase within a few days after a head injury may show an unstable vital sign, thus intensive monitoring of the vital sign and manual or mechanical ventilation during a MRI examination should be employed. Direct brain stem contusion has a good prognosis compared with brain stem injury associated with diffuse axonal injury (DAI). Small superficial lesions are detected only within a few days after a head injury. Recent studies of MRI in patients with head injuries could not determine the pathology. However, the differentiation of the pathophysiology must be clinically important because the prognoses are different and distinguishable using only acute stage MRI.

Decompressive craniectomy in severe traumatic brain injury - a study of 20 cases

Severe traumatic brain injury is common in all developing countries like Bangladesh. These patients are commonly managed conservatively in the most of the hospitals of our country where immediate surgical intervention and perioperative ICU facilities are not available.This cross sectional interventional study was aimed at evaluating and comparing the post operative surgical outcome of decompressive craniectomy in patients with severe traumatic brain injury (TBI) with conservatively treated patients.This study was done in Dhaka Medical College Hospital from January 2010 to December 2012. Twenty clinically suspected patients who sustained severe head injury with a GCS of 3-8 with neurological deterioration and evidence of brain contusion, laceration or evidence of brain swelling on CT Scan were included. Patient with primary fatal brain stem injury, an initial and persisting GCS score of 3, or bilaterally dilated and fixed pupil are not candidate for operative management. Outcome was assessed by Glasgow outcome scale (GOS). Follow up was given for a period of six to twelve months. DOI: http://dx.doi.org/10.3329/bmj.v43i2.21392 Bangladesh Med J. 2014 May; 43 (2): 100-102

Risk factors for intraoperative encephalocele in brain injury patients

Objective To explore the risk factors of acute intraoperative encephalocele in craniotomy of brain injury patients.Methods Gender,age,history of hypertension,hypotension,hypoxemia,primary brainstem injury,cerebral hernia,brain edema,time from injury to surgery,skull surgery distant sites fractur and bleeding situation were recorded and analyzed in 190 patients with acute intraoperative encephalocele and 506 patients without encephalocele.Results Distant sites fractured and bleeding,brain edema,cerebral hernia,hypoxemia,primary brainstem injury,time from injury to surgery,were closely related to the acute intraoperative encephalocele(P ＜ 0.05).Conclusions Skull surgery distant sites fracture,hypoxemia,primary brainstem injury,cerebral hernia,brain edema,and surgery distant sites bleeding situation (epidural hematoma) are the risk factors for the acute intraoperative encephalocele,that the time from injury to surgery is a protective factor.Actively correct hypoxia,primary brainstem injury and prevent secondary damage,prevention of distant sites bleeding situation can effectively reduce intraoperative encephalocele. Key words: Traumatic brain injury; Neurosurgical procedures; Encephalocele; Risk factors

Expression of amyloid-β protein and amyloid-β precursor protein after primary brain-stem injury in rats.

Amyloid-β (Aβ) protein and its precursor, amyloid-β precursor protein (β-APP), have traditionally been used in the diagnosis of Alzheimer disease. Their use in diagnosis of traumatic brain injury by forensic analysis is becoming more widespread. However, to date, no reliable small animal model exists to evaluate these brain injury indicators. To address this, we have studied primary brain-stem injury in rats to assess the appearance of diffuse axonal injury in brain sections and correlate these findings with appearance of Aβ and relative β-APP mRNA levels. Using an EnVision 2-step immunohistochemical staining method to measure axon diameter, we found that there was significant difference in axon diameters within the medulla oblongata and several time points after brain injury, ranging from 3 to 24 hours. In addition, mRNA expression levels of β-APP increased following brain injury, peaking 3 hours following injury and decreasing back to baseline levels by 24 hours after injury. These results suggest that using immunohistochemistry and reverse transcription-polymerase chain reaction to detect changes in Aβ-associated axonal changes and β-APP mRNA levels, respectively, can be useful for the diagnosis of diffuse axonal injury during autopsy at early time points following fatal brain injury.

外傷による一次性／二次性脳幹損傷のMRI 所見と予後

外傷による一次性／二次性脳幹損傷のMRI 所見と予後

Zolpidem Arouses Patients in Vegetative State After Brain Injury: Quantitative Evaluation and Indications

BackgroundTo investigate the efficacy and indications of Zolpidem, a nonbenzodiazepine hypnotic, inducing arousal in vegetative state patients after brain injury. MethodsOne hundred sixty-five patients were divided into 4 groups, according to area of brain damage and injury mechanism. All patients' brains were imaged by 99mTc-ECD single-photon emission computerized tomography (SPECT), before and 1hour after treatment with 10mg of zolpidem. Simultaneously, 3 quantitative indicators of brain function and damage were obtained using cerebral state monitor. Thirty-eight patients withdrew from the study after the first zolpidem dose. The remaining 127 patients received a daily dose of 10mg of zolpidem for 1week and were monitored again at the end of this week. ResultsOne hour after treatment with zolpidem, cerebral state index was increased and burst suppression reduced in both brain contrecoup contusion and space-occupying brain compression groups (P < 0.05). SPECT showed, 1hour after medication, that cerebral perfusion was improved in both brain contrecoup contusion and space-occupying brain compression groups, but no changes were seen in primary and secondary brain stem injury groups. In the 127 patients' group, after 1week of zolpidem treatment, all parameters obtained from cerebral state monitor were not statistically different compared with those after the initial medication (P > 0.05). ConclusionsZolpidem is an effective medicine to restore brain function in patients in vegetative state after brain injury, especially for those whose brain injuries are mainly in non-brain-stem areas. improvement of brain function is sudden rather than gradual.

Profile of Traumatic Brain Stem Injury: An Autopsy Study of 41 Cases

It is a prospective study of 41 cases of traumatic brain stem injury cases whose medico legal autopsy was done in the Institute of Forensic Medicine, at the Madras Medical College and Government General Hospital, Chennai from December 2007 to June 2008. In the 41 cases, 16 cases, (39.02%) were primary brain stem injury and 25 cases, (60.98) were secondary brain stem injury. The mean ages of cases with primary and secondary brainstem injuries were respectively 55.7 and 36.2. Male victims outnumbered the female victims with male female sex ratio of 13:1. Road traffic accidents involving mainly pedestrians and two wheelers were the most common cause for traumatic brain injury.

Pathological and immunohistochemical study of lethal primary brain stem injuries

BackgroundMany of the deaths that occur shortly after injury or in hospitals are caused by mild trauma. Slight morphological changes are often found in the brain stems of these patients during autopsy. The purpose of this study is to investigate the histopathological changes involved in primary brain stem injuries (PBSI) and their diagnostic significance.MethodsA total of 65 patients who had died of PBSI and other conditions were randomly selected. They were divided into 2 groups, an injury group (25 cases) and a control group (20 cases). Slides of each patient’s midbrain, pons, and medulla oblongata were prepared and stained with HE, argentaffin, and immunohistochemical agents (GFAP, NF, amyloid-ß, MBP). Under low power (×100) and NF staining, the diameter of the thickest longitudinal axon was measured at its widest point. Ten such diameters were collected for each part of the brain (midbrain, pons, and medulla oblongata). Data were recorded and analyzed statistically.ResultsBrain stem contusions, astrocyte activity, edema, and pathological changes in the neurons were visibly different in the injury and control groups (P < 0.05). Characteristic changes occurred in the neural axons, axon diameter varied from axon to axon and even over different segments of one axon, and several pathological phenomena were observed. These included segmental thickening and curving, wave-like processing, disarrangement, and irregular swelling. A few axons ruptured and intumesced into retraction balls. Immunohistochemical MBP staining showed enlargement and curving of spaces between the myelin sheaths and axons in certain areas. The myelin sheaths lining the surfaces of the axons were in some cases incomplete and even exfoliated, and segmentation disappeared. These pathological changes increased in severity over time (P < 0.05).ConclusionsThese histopathological changes may prove beneficial to the pathological diagnosis of PBSI during autopsy. The measurement of axon diameters provides a referent quantitative index for the diagnosis of the specific causes of death involved in PBSI.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1345298818712204

Clinical analys of 28 cases with severe craniocerebral injury hyponatremia

Objective To research the of etiology,pathogenesis,diagnosis,and treatment.Severe head trauma research with hyponatremia.Methods A retrospective hospital in January 2008-2009 December severe head trauma 28 patients with hyponatremia in the diagnosis and treatment of patients.Results SIADHS,4 cases diagnosed by water treatment,24 patients were serum sodium,23 patients were diagnosed CSWS at 10 d treatment for expansion,and to added sodium,improved,1 cases of primary brainstem injury MODS concurrent and death.Conclusion cerebal saltwasting syndrome of inappropriate secretion of antidiuretic hormone secretion with abnormal syndrome pathogenesis and treatment measures are completely different,grasp type and improve outcomes have very important significance. Key words: Severe; Craniocerebral trauma; Hyponatremia; Diagnosis; Treatment

Clinical analysis of 326 cases of early death of acute closed craniocerebral trauma

Objective To summarize the clinical characteristics and management of cases of early death of acute closed craniocerebral trauma. Methods The clinical data of 326 early death ( within 1 week) cases of acute closed severe traumatic brain injury were studied retrospectively to identify the main causes of death in acute phase. Results The main causes of early death were refractory high intracranial pressure because of intracranial hematoma, cerebral ischemia, cerebral edema. The main causes of early death included: Refractory intracranial hypertension leading to brain herniation (82％), other systemic complications (8％) , primary brain stem injury( 6％ ) and acute hemorrhagic shock(4％). 58％ death due to refractory intracranial hypertension occured within 2 days. The cause of 133 postoperative death was refractory intracranial hypertension. Conclusions The main cause of early death of acute closed craniocerebral trauma is refractory intracranial hypertension. It is very important to find the cause of refractory intracranial hypertension for early prevention and therapy. Key words: Craniocerebral trauma; Cause of beath; Intracranial hypertension

Pathologic and immunohistochemical study on lethal primary brain stem injury

To study the histopathologic changes of primary brain stem injury and to investigate their significance in the diagnosis of primary brain stem injury. Sixty-five autopsy cases died of primary brain stem injury and other diseases were enrolled into this study. The cases were subdivided into brain stem injury group (n = 25) and control group (including 20 cases died of cardiovascular disease and 20 cases died of non-cardiovascular diseases). The brain stem tissue sections were stained with hematoxylin-eosin and silver impregnation techniques. Immunohisto chemical study for glial fibrillary acidic protein, neurofilament, amyloid-beta and myelin basic protein was carried out. The widest cross diameters of 10 axons highlighted by immunostaining were measured in each low power field (x 100) through light miscroscopy in all the cases studied. In comparing with that of the control group, there were differences in the degree of contusion lesion, reactive astrocytosis, edema and pathologic changes of neuronal cells present in the brain stem injury group and was statistically significant (P < 0.05). The axons locating in the brain stem injury group showed a distinctive histology by the appearance of significantly larger diameters (P < 0.05). Primary brain stem injury demonstrates certain distinctive histopathologic changes and measurement of axonal diameters provides an additional quantitative index useful in autopsy diagnosis.