Auditory pathways fail to re-establish normal cortical activation patterns in response to binaural stimulation following a unilateral lesion of the inferior colliculus.

The aim of this study was to investigate cortical activation in response to binaural stimulus presentations in an individual (FX) with a circumscribed traumatic hemorrhagic lesion of the right inferior colliculus. FX and control subjects were exposed to complex sounds while undergoing a functional magnetic resonance imaging assessment. Whereas normally-hearing individuals show well-balanced bilateral activation patterns in response to binaural auditory stimulation, the same stimuli produced stronger activation in the left hemisphere in FX. Combined with previous data, these findings reinforce the notion that the inferior colliculus is an essential auditory relay and that its loss cannot be significantly compensated.

[Early disturbances of gastric myoelectrical activity in a patient with brainstem hematoma. Case report]. / Wczesne zaburzenia aktywnosci mioelektrycznej zoladka u chorego z krwiakiem pnia mózgu. Opis przypadku.

Described early disturbances of gastric myoelectrical activity in 18-years old patient, which appeared immediately after craniocerebral trauma. Brain MRI in a patient showed brainstem hematoma. Bradygastria amounts to 53.6% of the recording time.

Brainstem hemorrhage in descending transtentorial herniation (Duret hemorrhage).

OBJECTIVES: To review clinical and radiological findings in patients with Duret hemorrhages and to discuss the pathophysiology and differential diagnosis of these lesions. PATIENTS AND METHODS: We reviewed the case records of four patients with Duret hemorrhages who had been admitted to the neurological intensive care unit with supratentorial mass lesions. RESULTS: Descending transtentorial and subfalcine herniations were present in all cases. Three patients were admitted with acute subdural hematoma and one with intraparenchymal hemorrhage. Computed tomography revealed the presence of blood in the mesencephalon and upper pons. Three patients died; one survived with severe disabilities. DISCUSSION: Duret hemorrhages are typically located in the ventral and paramedian aspects of the upper brainstem (mesencephalon and pons). The pathophysiology of Duret hemorrhage remains under debate: arterial origin (stretching and laceration of pontine perforating branches of the basilar artery), versus venous origin (thrombosis and venous infarction). Multifactorial causation seems likely. CONCLUSION: Duret hemorrhages are delayed, secondary brainstem hemorrhages. They occur in craniocerebral trauma victims with rapidly evolving descending transtentorial herniation. Diagnosis is made on computed tomography of the brain. In most cases the outcome is fatal. On the basis of our observations we believe that arterial hypertension and advanced age are risk factors for the development of Duret hemorrhage.

Roles of glutamate transporter and receptors, poly (ADPribose) polymerase, and transforming growth factor-beta1 in pontosubicular neuron necrosis.

The expression of neuron-type glutamate transporters (EAAC-1), AMPA glutamate receptor subunits (GluR1 and GluR2/3), polyadenosine (5'diphosphate-ribose) polymerase (PARP), and transforming growth factor-beta1 was investigated in 20 cases of neonatal pontosubicular neuron necrosis and 12 gestational-age matched controls. Developmental immunoreactivities of EAAC-1, GluR1, and GluR2/3 appeared in the neurons of the pontine nuclei at 29 to 30 weeks' gestation in controls, and then gradually increased with age. However, these activities were decreased in the pontine nucleus of patients with pontosubicular neuron necrosis. Decreases in these immunoreactivities might indicate early degeneration of neurons. Although PARP and transforming growth factor-beta1 immunoreactivity was insignificant or very weak in the pontine nuclei at any age in controls, PARP was markedly expressed in karyorrhectic neurons of the pontine nucleus in patients with pontosubicular neuron necrosis. Transforming growth factor-beta1 immunoreactivity was observed in nonkaryorrhectic neurons of the pontine nuclei. PARP could contribute to the pathogenesis of pontosubicular neuron necrosis more than EAAC-1 or GluR1 or GluR2/3. Transforming growth factor-beta1 could play a role in the protection and repair of damaged neurons.