Duret Brainstem Hemorrhage After Transtentorial Descending Brain Herniation: A Systematic Review and Meta-Analysis.

BACKGROUND: Historically, the occurrence of hemorrhage in the brainstem after an episode of supratentorial intracranial hypertension was described by Henri Duret in 1878. Nevertheless, to date the eponym Duret brainstem hemorrhage (DBH) lacks systematic evidence regarding its epidemiology, pathophysiology, clinical and radiologic presentation, and outcome. METHODS: We conducted a systematic literature review and meta-analysis using the Medline database from inception to 2022 looking for English-language articles concerning DBH, in accordance with the PRISMA guidelines. RESULTS: The research yielded 28 articles for 32 patients (mean age, 50 years; male/female ratio, 3:1). Of patients, 41% had head trauma causing 63% of subdural hematoma, responsible for coma in 78% and mydriasis in 69%. DBH appeared on the emergency imaging in 41% and on delayed imaging in 56%. DBH was located in the midbrain in 41% of the patients, and in the upper middle pons in 56%. DBH was caused by sudden downward displacement of the upper brainstem secondary to supratentorial intracranial hypertension (91%), intracranial hypotension (6%), or mechanical traction (3%). Such downward displacement caused the rupture of basilar artery perforators. Brainstem focal symptoms (P = 0.003) and decompressive craniectomy (P = 0.164) were potential favorable prognostic factors, whereas an age >50 years showed a trend toward a poor prognosis (P = 0.0731). CONCLUSIONS: Unlike its historical description, DBH appears as a focal hematoma in the upper brainstem caused by the rupture of anteromedial basilar artery perforators after sudden downward displacement of the brainstem, regardless of its cause.

Deferoxamine Alleviates Iron Overload and Brain Injury in a Rat Model of Brainstem Hemorrhage.

BACKGROUND: Brainstem hemorrhage (BSH) is the most dangerous and devastating subtype of intracerebral hemorrhage and is associated with high morbidity and mortality. However, to date, no effective prevention methods or specific therapies have been available to improve its clinical outcomes. We preliminarily explored the efficacy of deferoxamine (DFO), a clinical chelator known for its iron-scavenging activities, in a rat model of BSH induced with collagenase infusion. METHODS: DFO or saline was administrated 6 hours after BSH induction and then every 12 hours for ≤7 days. The survival curve of the rats was created, and the neurological scores were examined on days 1, 3, and 7 after BSH. The rats were sacrificed after 1, 3, and 7 days of DFO treatment for histological examination and immunohistochemistry. RESULTS: The results showed that administration of DFO delayed erythrocytes lysis, reduced iron deposition, reduced reactive oxygen species generation, reduced heme oxygenase-1 expression, and alleviated brain injury such as neuron degeneration and myelin sheath injury. However, DFO did not improve the survival rate and neurobehavioral outcomes in this model. CONCLUSIONS: Administration of DFO had limited therapeutic effects on collagenase-induced brainstem hemorrhage in rats. Some potential explanations were proposed, and more preclinical work is required to clarify the controversial curative effect of DFO in ICH.

Hemorragia vítrea bilateral asociada a hemorragia pontomesencefálica: un caso extremo de síndrome de Terson / Bilateral vitreous haemorrhage associated with pontomesencephalic haemorrhage: an extreme case of Terson syndrome

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Hypertrophic olivary degeneration secondary to pontine haemorrhage.

We report a 58-year-old man who developed hyptertrophic olivary degeneration (HOD) after haemorrhage of a cavernous malformation in the pons. Lesions of the triangle of Guillain and Mollaret (the dentatorubro-olivary pathway) may lead to HOD, a secondary transsynaptic degeneration of the inferior olivary nucleus. HOD is considered unique because the degenerating olive initially becomes hypertrophic rather than atrophic. The primary lesion causing pathway interruption is often haemorrhage, either due to hypertension, trauma, surgery or, as in our patient, a vascular malformation such as a cavernoma. Ischaemia and demyelination can also occasionally be the inciting events. The classic clinical presentation of HOD is palatal myoclonus, although not all patients with HOD develop this symptom. The imaging features of HOD evolve through characteristic phases. The clue to the diagnosis of HOD is recognition of the distinct imaging stages and identification of a remote primary lesion in the triangle of Guillain and Mollaret. Familiarity with the classic imaging findings of this rare phenomenon is necessary in order to avoid misdiagnosis and prevent unnecessary intervention.

Micronystagmus of oculopalatal tremor.

Three months after brainstem hemorrhage, MRI revealed a hyperintense lesion of the left inferior olivary nucleus of a 45-year-old man (figure). The patient was completely asymptomatic, but exhibited oculopalatal tremor (OPT), rhythmic palatal oscillations, and small-amplitude vertical pendular nystagmus of the right eye, best visualized on fundus examination (see video).

Dystonia associated with pontomesencephalic lesions.

Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4-56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits.

Survival with good outcome after cerebral herniation and Duret hemorrhage caused by traumatic brain injury.

Brainstem hemorrhage can occur as a primary or secondary event in traumatic brain injury (TBI). Secondary brainstem hemorrhage that evolves from raised intracranial pressure and transtentorial herniation is referred to as Duret hemorrhage. Duret hemorrhage following TBI has been considered an irreversible and terminal event. The authors report on the case of a young adult patient with TBI who presented with a low Glasgow Coma Scale score and advanced signs of cerebral herniation. She underwent an urgent decompressive hemicraniectomy for evacuation of an acute epidural hematoma and developed a Duret hemorrhage postoperatively. In accordance with the family's wishes, aggressive TBI monitoring and treatment in the intensive care unit was continued even though the anticipated outcome was poor. After a lengthy hospital course, the patient improved dramatically and was discharged ambulatory, with good cognitive functioning and a Glasgow Outcome Scale score of 4. Duret hemorrhage secondary to raised intracranial pressure is not always a terminal event, and by itself should not trigger a decision to withdraw care. Aggressive intracranial monitoring and treatment of a Duret hemorrhage arising secondary to cerebral herniation may enable a good recovery in selected patients after severe TBI.

Traumatic midbrain hematoma in a patient presenting with an isolated palsy of voluntary facial movements. Case report.

The authors report on the case of a young man with a mild head injury and an isolated palsy of voluntary facial movements, attributed to a midbrain traumatic hematoma. This exception to the generally accepted conjunction between brainstem contusion and poor prognosis pertains to a special entity of midbrain laceration due to hyperextension of the head, with minimal influence on the level of consciousness. The clinical presentation of this lesion with facial palsy sparing emotion-related movement has rarely been described and offers a clue for exploring the neuroanatomy of facial movement.

Midbrain hemorrhage presenting with oculomotor nerve palsy: case report.

BACKGROUND: We report a case of isolated oculomotor nerve palsy caused by a midbrain hemorrhage. CASE DESCRIPTION: A 75-year-old man visited our hospital complaining of double vision and left eye ptosis without headache. Neuro-ophthalmic examination showed that his left and right pupils were 3.5 mm and 3 mm in diameter, respectively, that left downward eye movement was limited, and that convergence of the right eye was limited. Magnetic resonance imaging (MRI) demonstrated that there was a hematoma located in the anterior tegmentum of the left midbrain. Two weeks after admission and treatment, including conservative therapy, his double vision gradually disappeared. CONCLUSION: To date, 73 cases have been reported in the literature. Most cases of isolated oculomotor nerve palsy have been caused by diabetes mellitus, aneurysm, or infarction. However, focal midbrain hemorrhage incidentally produces third nerve palsy. MRI is extremely helpful in diagnosing a small hemorrhage of the midbrain in such cases.