Transtentorial Brain Herniation Research Articles

Emergency decompressive surgery in patients with transtentorial brain herniation and pupillary abnormalities: the importance of improved pupillary response after osmotherapy and surgery.

The predictors of survival and functional recovery following emergency decompressive surgery in patients with transtentorial brain herniation, particularly those with pupillary abnormalities, have not been established. In this study, the authors aimed to assess the outcome of patients with intracranial mass lesions, transtentorial brain herniation, and nonreactive mydriasis, following emergency surgical decompression. A retrospective chart review was performed of all patients with transtentorial herniation and pupillary abnormalities who underwent craniotomy or craniectomy at two trauma and stroke centers between 2016 and 2022. The functional outcome was determined using the modified Rankin Scale (mRS). Forty-three patients, 34 men and 9 women with a mean age of 47 years (range 16-92 years), were included. The underlying etiology was traumatic brain injury in 33 patients, hemorrhagic stroke in 8 patients, and tumor in 2 patients. The median preoperative Glasgow Coma Scale score was 3 (range 3-8), and the median midline shift was 9 mm (range 1-29 mm). Thirty-two patients (74.4%) had bilaterally fixed and dilated pupils. The median time to surgery (from pupillary changes) was 133 minutes (mean 169 minutes, range 30-900 minutes). Eighteen patients (41.9%) died postoperatively. After a median follow-up of 12 months (range 3-12 months), 11 patients (26.8%) had a favorable functional outcome, while 10 remained severely disabled (mRS score 5). On univariate analysis, younger age (p < 0.001), less midline shift (p = 0.049), and improved pupillary response after osmotic therapy (p < 0.01) or decompressive surgery (p < 0.001) were associated with favorable outcomes at 3 months. With aggressive medical and surgical management, patients with transtentorial brain herniation, including those with bilaterally fixed and dilated pupils, may have considerable rates of survival and functional recovery. Young age, less midline shift, and improved pupillary response following osmotic therapy or decompressive surgery are favorable prognosticators.

The Kinetics of Transtentorial Brain Herniation: Kernohan-Woltman Notch Phenomenon Revisited.

To critically review recent literature in understanding the pathological consequences of transtentorial brain herniation resulting from unilateral expanding supratentorial mass lesions. Modern neuroimaging assists in understanding the consequences of transtentorial brain herniation with the development of the Kernohan-Woltman notch phenomenon. MRI studies in post-operative patients undergoing craniotomy and removal of expanding unilateral hemispheric mass lesions (usually an extradural or subdural hematoma) have shown striking findings in the contralateral crus cerebri suggestive of damage as a result of impact against the free margin of the opposite tentorium as suggested by Kernohan and Woltman nearly a century back in autopsy studies. MR changes include T1 hypointensity, T2 and fluid-attenuated inversion recovery (FLAIR) hyperintensity, DW1 hyperintensity with restriction of diffusion, presence of hypointensity in GRE sequences and evidence of axonal damage in the corticospinal tracts in the cerebral peduncle in diffusion tensor imaging and MR tractography. The pathological basis of such changes may be variable or a combination of several pathological processes, which may all be related to the impact/compression of the contralateral crus with the tentorial margin. These include contusion, compression, demyelination, and perhaps most importantly microvascular damage including microbleeds. The role of uncal herniation is debatable. It appears that as a result of massive lateral shift in the supratentorial compartment, there is a transient forceful impact of the opposite cerebral peduncle against the rigid tentorial border to induce one or more of the abovementioned phenomena to explain the imaging findings. The limitation of these studies is that most of them have been done in the post-operative periods and surgical manipulations can surely alter anatomical relationships between intracranial structures. The exact sequence of events happening intracranially in the face of rapidly expanding supratentorial mass lesions is largely unknown. Even with rapid progress in neuroimaging, documentation of such changes during life are difficult, principally for logistic reasons. Consequently, the very truth of the much taught about phenomenon of uncal herniation and the resultant Kernohan-Woltman notch phenomenon and the false localizing sign of unilateral motor weakness and contralateral pupillary dilation have been questioned. Animal experimentation and autopsy studies have not contributed much in our understanding of the actual process happening intracranially in such an emergent situation. The midbrain undoubtedly is the key structure bearing the brunt of the effect of brain shift which is more lateral than downward in cases with unilateral expanding lesions. Structural changes in the cerebral peduncles have now been visualized with modern neuroimaging. These alterations may result from the interplay of one or more factors which include compression, contusion, demyelination, and perhaps most importantly microvascular ischemia and hemorrhage resulting from a forceful yet transient impact of the cerebral peduncle with the tough tentorial margin. The last mentioned hypothesis would be in conformity with Kernohan and Woltman's concept of elastic deformation of the midbrain. In the present article an attempt is made to provide a historical account of the changing concepts in relation to brain herniation as systematically and chronologically as possible, and then, critically review recent neuroimaging observations with a view to hypothesize on the sequence of events during transtentorial brain herniation.

Duret Brainstem Hemorrhage Secondary to Large Supratentorial Meningioma

A 75-year-old female patient was admitted following head trauma responsible for an acute-onset neurological worsening with a Glasgow Coma Scalescore of 6. Computed tomography scan revealed a large bifrontal meningioma with extralesional bleeding causing cranio-caudal transtentorial brain herniation. Despite emergency surgical excision of the tumor using craniotomy, the patient remained comatose. The brain magnetic resonance imaging revealed a Duret brainstem hemorrhage of the upper and middle pons, associated with supratentorial decompression-related brain injuries. One month later, the patient was withdrawn from life support. To our knowledge, tumor-induced Duret brainstem hemorrhage has never been reported.

Brain Death Diagnosis in Primary Posterior Fossa Lesions.

New controversies have raised on brain death (BD) diagnosis when lesions are localized in the posterior fossa. The aim of this study was to discuss the particularities of BD diagnosis in patients with posterior fossa lesions. The author made a systematic review of literature on this topic. A supratentorial brain lesion usually produces a rostrocaudal transtentorial brain herniation, resulting in forebrain and brainstem loss of function. In secondary brain lesions (i.e., cerebral hypoxia), the brainstem is also affected like the forebrain. Nevertheless, some cases complaining posterior fossa lesions (i.e., basilar artery thrombotic infarcts, or hemorrhages of the brainstem and/or cerebellum) may retain intracranial blood flow and EEG activity. In this article, I discuss that if a posterior fossa lesion does not produce an enormous increment of intracranial pressure, a complete intracranial circulatory arrest does not occur, explaining the preservation of EEG activity, evoked potentials, and autonomic function. I also addressed Jahi McMath, who was declared braindead, but ancillary tests, performed 9 months after initial brain insult, showed conservation of intracranial structures, EEG activity, and autonomic reactivity to "Mother Talks" stimulus, rejecting the diagnosis of BD. Jahi McMath's MRI study demonstrated a huge lesion in the pons. Some authors have argued that in patients with primary brainstem lesions it might be possible to find in some cases partial recovery of consciousness, even fulfilling clinical BD criteria. This was the case in Jahi McMath.

In Reply to the Letter to the Editor Regarding ‘Transtentorial Brain Herniation After Lumbar Drainage in Patient Planned for Cranioplastic Reconstruction: Catastrophic Play Between Atmospheric and Intracranial Pressure’

Cerebral vasospasm and delayed ischemic neurologic deficits are well-known clinical aftereffects of subarachnoid hemorrhage due to rupture of an intracranial aneurysm. However, vasospasm with consequential ischemia after clipping of an unruptured aneurysm is an exceedingly rare sequela encountered in the reported neurosurgical literature.A 53-year-old woman had presented for elective craniotomy with microsurgical clipping of an unruptured left middle cerebral artery bifurcation saccular aneurysm, which was successfully treated without complications. Despite an initially benign clinical course, she experienced diffuse vasospasm with profound ischemic neurologic deficits on postoperative day 13 with a left middle cerebral artery distribution ischemic infarct. Moreover, she developed recurrent delayed spasm of the right posterior cerebral artery on postoperative day 26 and, consequentially, a left homonymous hemianopsia despite treatment with intra-arterial verapamil infusion.To the best of our knowledge, we have reported the first case of recurrent cerebral vasospasm and delayed ischemia neurologic deficits weeks subsequent to clipping of an unruptured aneurysm. The findings from the present case highlight the importance of considering delayed vasospasm as a cause of acute onset neurologic symptoms for patients who have recently undergone elective aneurysm surgery. We also reviewed the current data regarding the epidemiology, surgical factors, and proposed pathophysiologic mechanisms related to vasospasm after elective cases.

Letter to the Editor Regarding “Transtentorial Brain Herniation After Lumbar Drainage in Patient Planned for Cranioplastic Reconstruction: Catastrophic Play Between Atmospheric and Intracranial Pressure”

Letter to the Editor Regarding “Transtentorial Brain Herniation After Lumbar Drainage in Patient Planned for Cranioplastic Reconstruction: Catastrophic Play Between Atmospheric and Intracranial Pressure”

Secondary (Duret) brainstem haemorrhage may not always represent a fatal event

Background. Secondary brainstem haemorrhage (eponymously called Duret haemorrhage) is a well-known complication of transtentorial brain herniation or of rapid decompression of intracranial space. It is considered to be a consequence of arterial rupture, venous infarction or ischemia-reperfusion injury and it is regarded as a harbinger of an unfavourable outcome for the patient. Despite this, several case reports describing good outcome after Duret haemorrhage preceded by evacuation of an expansive traumatic intracranial mass lesion, an episode of intracranial hypotension or lumbar drainage have been published.Case description. We present four cases of patients with secondary brainstem haemorrhage linked to an episode of intracranial hypertension due to various reasons who were treated at our clinic. The first patient suffered a small brainstem haemorrhage that was described on his initial CT scan presumably as a result of massive intracranial expansion caused by an acute subdural haematoma and this Duret haemorrhage markedly expanded after the subdural haematoma was evacuated by means of a decompressive craniectomy. The next two patients developed Duret haemorrhage after the evacuation of intracranial haematomas. The fourth patient presented with posttraumatic cerebral oedema complicated by a subtle Duret haemorrhage displayed on his initial CT scan and this bleeding remained stable even after a bilateral decompressive craniectomy. One patient passed away, one remained in a persistent coma and two survived with a light neurological deficit.Conclusions. However ominous a newly discovered Duret haemorrhage may be, it alone should not discourage us from the further intensive treatment of our patients as their outcome may considerably vary. The extent of this bleeding, type and severity of underlying brain injury and complete clinical status and history of our patients should all be taken into account when deciding about patients’ prognosis.

Automated Pupillometry and Detection of Clinical Transtentorial Brain Herniation: A Case Series.

Transtentorial herniation (TTH) is a life-threatening neurologic condition that typically results from expansion of supratentorial mass lesions. A change in bedside pupillary examination is central to the clinical diagnosis of TTH. Materials and. To quantify the changes in the pupillary examination that precede and accompany TTH and its treatment, we evaluated 12 episodes of herniation in three patients with supratentorial mass lesions using automated pupillometry (NeurOptics, Inc., Irvine, CA). Herniation was defined clinically by the onset of fixed and dilated pupils in association with decreased levels of consciousness. Automated pupillometry was measured simultaneously with the bedside clinical examination, but the clinical team was blinded to these results and could not act on the data. Data from the pupillometer were downloaded 1-2 times per week onto a secured laptop, and data processing was facilitated by the use of Mathematica 8.0. Neurologic Pupil Index measurements, values generated by the pupillometer based on an algorithm that incorporates pupillary size and reactivity in a normal population, were found to be abnormal before 73% of TTHs. This abnormality occurred at a median of 7.4 h before TTH. All episodes of TTH were reversed after clinical intervention at a median of 43 min after the event. The value did not fall to 0 in 42% of clinical herniations, but it did decrease to very abnormal values of 0.5-0.8. The potential of automated pupillometry to guide the management of severely injured neurologic patients is intriguing and warrants further study in the critical care unit and beyond. The utility of a portable device in the combat setting may allow for triage of patients with severe neurologic injury.

Brainstem Monitoring in the Neurocritical Care Unit: A Rationale for Real-Time, Automated Neurophysiological Monitoring.

Patients with severe traumatic brain injury or large intracranial space-occupying lesions (spontaneous cerebral hemorrhage, infarction, or tumor) commonly present to the neurocritical care unit with an altered mental status. Many experience progressive stupor and coma from mass effects and transtentorial brain herniation compromising the ascending arousal (reticular activating) system. Yet, little progress has been made in the practicality of bedside, noninvasive, real-time, automated, neurophysiological brainstem, or cerebral hemispheric monitoring. In this critical review, we discuss the ascending arousal system, brain herniation, and shortcomings of our current management including the neurological exam, intracranial pressure monitoring, and neuroimaging. We present a rationale for the development of nurse-friendly-continuous, automated, and alarmed-evoked potential monitoring, based upon the clinical and experimental literature, advances in the prognostication of cerebral anoxia, and intraoperative neurophysiological monitoring.

Diagnosis and treatment of hyponatraemia in neurosurgical patients

Hyponatraemia is the most common electrolyte imbalance in neurosurgical patients. Acute hyponatraemia is particularly common in neurosurgical patients after any type of brain insult, including brain tumours and their treatment, pituitary surgery, subarachnoid haemorrhage or traumatic brain injury. Acute hyponatraemia is an emergency condition, as it leads to cerebral oedema due to passive osmotic movement of water from the hypotonic plasma to the relatively hypertonic brain which ultimately is the cause of the symptoms associated with hyponatraemia. These include decreased level of consciousness, seizures, non-cardiogenic pulmonary oedema or transtentorial brain herniation. Prompt treatment is mandatory to prevent such complications, minimize permanent brain damage and therefore permit rapid recovery after brain insult. The infusion of 3% hypertonic saline is the treatment of choice with different rates of administration based on the severity of symptoms and the rate of drop in plasma sodium concentration.The pathophysiology of hyponatraemia in neurotrauma is multifactorial; although the syndrome of inappropriate antidiuresis (SIADH) and central adrenal insufficiency are the commonest causes encountered. Fluid restriction has historically been the classical treatment for SIADH, although it is relatively contraindicated in some neurosurgical patients such as those with subarachnoid haemorrhage. Furthermore, many cases admitted have acute onset hyponatraemia, who require hypertonic saline infusion. The recently developed vasopressin receptor 2 antagonist class of drug is a promising and effective tool but more evidence is needed in neurosurgical patients. Central adrenal insufficiency may also cause acute hyponatraemia in neurosurgical patients; this responds clinically and biochemically to hydrocortisone. The rare cerebral salt wasting syndrome is treated with large volume normal saline infusion. In this review, we summarize the current evidence based on the clinical presentation, causes and treatment of different types of hyponatraemia in neurosurgical patients.

Pediatric Brain Death: Updated Guidelines

Logan, a 5-year-old boy, was riding his bike with his 7-year-old brother when he was struck from behind by a car traveling at approximately 40 mph. The driver indicated that she did not see the riders until she hit Logan, who was not wearing a helmet at the time of the accident. Logan was thrown from his bike and was found at the side of the road, unresponsive and posturing. Although he was uninjured, Logan’s brother witnessed the incident.Emergency medical services arrived and placed Logan on a backboard with a c-collar. Because he was not protecting his airway, he was intubated and then given sodium chloride fluids and brought to the pediatric emergency department. Upon arrival, his Glasgow Coma Scale score was 5, and his right pupil was 6 mm and not reactive.Logan’s initial head computed tomographic scan showed diffuse brain edema, with early downward transtentorial brain herniation. The pediatric neurosurgeon determined that no operative management was appropriate for Logan. Besides a small laceration on his forehead, Logan had no other injuries. At this time, he was taking a few spontaneous respirations and had occasional posturing of his extremities.

Pediatric Brain Death

Logan, a 5-year-old boy, was riding his bike with his 7-year-old brother when he was struck from behind by a car traveling at approximately 40 mph. The driver indicated that she did not see the riders until she hit Logan, who was not wearing a helmet at the time of the accident. Logan was thrown from his bike and was found at the side of the road, unresponsive and posturing. Although he was uninjured, Logan's brother witnessed the incident.Emergency medical services arrived and placed Logan on a backboard with a c-collar. Because he was not protecting his airway, he was intubated and then given sodium chloride fluids and brought to the pediatric emergency department. Upon arrival, his Glasgow Coma Scale score was 5, and his right pupil was 6 mm and not reactive.Logan's initial head computed tomographic scan showed diffuse brain edema, with early downward transtentorial brain herniation. The pediatric neurosurgeon determined that no operative management was appropriate for Logan. Besides a small laceration on his forehead, Logan had no other injuries. At this time, he was taking a few spontaneous respirations and had occasional posturing of his extremities.

Cerebral edema and a transtentorial brain herniation syndrome associated with pandemic swine influenza A (H1N1) virus infection

Acute encephalitis, encephalopathy, and seizures are known rare neurologic sequelae of respiratory tract infection with seasonal influenza A and B virus, but the neurological complications of the pandemic 2009 swine influenza A (H1N1) virus, particularly in adults, are ill-defined. We document two young adults suffering from H1N1-associated acute respiratory distress syndrome and renal failure who developed cerebral edema. The patients acutely developed a transtentorial brain herniation syndrome including a unilateral third nerve palsy (dilated and unresponsive pupils), elevated intracranial pressure, coma, and radiological evidence of diffuse cerebral edema. In both patients, neurological deterioration occurred in the context of hyponatremia and a systemic inflammatory state. These patients illustrate that severe neurologic complications, including malignant cerebral edema, can occur in adults infected with H1N1 virus, and illustrate the need for close neurological monitoring of potential neurological morbidities in future pandemics.

Brain herniation in a patient with apparently normal intracranial pressure: a case report

IntroductionIntracranial pressure monitoring is commonly implemented in patients with neurologic injury and at high risk of developing intracranial hypertension, to detect changes in intracranial pressure in a timely manner. This enables early and potentially life-saving treatment of intracranial hypertension.Case presentationAn intraparenchymal pressure probe was placed in the hemisphere contralateral to a large basal ganglia hemorrhage in a 75-year-old Caucasian man who was mechanically ventilated and sedated because of depressed consciousness. Intracranial pressures were continuously recorded and never exceeded 17 mmHg. After sedation had been stopped, our patient showed clinical signs of transtentorial brain herniation, despite apparently normal intracranial pressures (less than 10 mmHg). Computed tomography revealed that the size of the intracerebral hematoma had increased together with significant unilateral brain edema and transtentorial herniation. The contralateral hemisphere where the intraparenchymal pressure probe was placed appeared normal. Our patient underwent emergency decompressive craniotomy and was tracheotomized early, but did not completely recover.ConclusionsIntraparenchymal pressure probes placed in the hemisphere contralateral to an intracerebral hematoma may dramatically underestimate intracranial pressure despite apparently normal values, even in the case of transtentorial brain herniation.

Variations in location of the arteries coursing between the brain stem and the free edge of the tentorium.

The locations of arterial branches crossing the free edge of the tentorium were studied in 16 adult cadavers. Two positional variants of the superior cerebellar artery and four variants of the posterior cerebral artery were identified. The points at risk of compression by different types of transtentorial brain herniation were defined for both the arterial branches supplying the brain stem and the arterial branches supplying the cerebral hemispheres.

Transtentorial Brain Herniation in the Monkey: Analysis of Brain Stem Auditory and Somatosensory Evoked Potentials

A monkey model of transtentorial brain herniation (TBH) was created to simulate the clinically encountered situation of a gradually expanding intracranial lesion. TBH was produced by extradural balloon inflation over a 4-hour period and documented by the appearance of the pupils as dilated or fixed at midposition. Intracranial pressure (ICP), brain stem auditory evoked potentials (BAEP), and short-latency somatosensory evoked potentials (SSEP) were recorded before, during, and after TBH. Statistical significance from baseline values to TBH was found for diminution of the BAEP amplitude, rise of the ICP, and diminution of the SSEP amplitude. An ICP rise to twice the baseline value and a 25% decrease in Wave V amplitude was found 1 hour before TBH. Changes in BAEP and SSEP took several minutes after deflation to return to baseline values. Analysis of Wave V of the BAEP was as sensitive as ICP in warning of TBH. Discussion centers upon previous animal studies of brain herniation and ICP elevation, and findings reported in humans deteriorating as a result of intracranial mass lesions. BAEP and SSEP monitoring may be used as noninvasive tests for brain stem compression in the setting of primate TBH, and in the future may be used to guide the effectiveness of therapy.