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The purpose of the present study was to further elucidate with the use of microstimulation techniques the influences of rostral pons and midbrain loci on the neuronal networks responsible for cortically induced rhythmical jaw movement (RJM) activity in the anesthetized guinea pig and to establish if these rostral brain-stem loci are capable of modulating the timing as well as the amplitude of rhythmical digastric (DIG) EMG activity. It was found that repetitive electrical stimulation of widespread areas of the rostral pons and mid-brain produced suppression of ongoing cortically induced rhythmical EMG activity. Prior to complete EMG suppression there was a reduction in amplitude of the DIG EMG and an increase in cycle duration. Repetitive stimulation of these suppressive loci also produced a reduction in the amplitude of the short-latency DIG EMG response produced by short pulse train stimulation of the masticatory cortex. This indicates that part of the suppression of cortically induced rhythmical EMG activity was due to a reduction in excitability of the polysynaptic short-latency pathway from cortex to DIG motoneurons. Short pulse train stimulation of these brain-stem suppressive loci during various phases of the rhythmical DIG cycle produced a phase-dependent increase in duration of the ongoing perturbed cycle. The cycles following the stimulus perturbation did not show any compensatory shortening in their durations suggesting that the stimulus produced a true resetting of the cycle. These data suggest that the brain-stem loci that produce suppression of RJMs evoked by repetitive cortical stimulation can affect the excitability of the central circuits responsible for cycle oscillation and timing as well as the excitability of the polysynaptic short-latency corticotrigeminal pathway to DIG motoneurons.
Auditory evoked brain-stem responses (ABRs) were recorded in 19 out of 52 brain dead cases in Department of Emergency Medicine, University of Tokyo Hospital from May, 1981 to January, 1984. The causes of brain death were severe head injury (9 cases), cerebro-vascular disease (7 cases), anoxia (2 cases), hydrocephalus (1 case). Eleven cases of them fulfilled the clinical criteria which included absence of cortical and brain-stem functions excluding severe hypothermia and depressant drug intoxication. The remainders who were subjected to barbiturate therapy were diagnosed as brain death for non-filling phenomenon in cerebral angiography. Results were as follows; Fourteen cases (74%) had no identifiable ABR waves. One case (5%) had only 1st wave. Three cases (16%) had 1st and 2nd waves. One case (5%) had 1st, 2nd, and 3rd waves. In spite of definition of clinical brain death, 5 cases had at least 1st wave, and therefore these datum suggested that ABR might have less clinical utility in diagnosis of brain death. Each case did not necessarily demonstrate the total extinction of ABRs, as was shown in (2) to (4) mentioned above. The clinical status which met the criteria of brain death might therefore possibly imply any conditions in which brain death was impending gradually to result in the total brain death of cerebrum through medulla oblongata. Under these circumstances, how barbiturate might produce ABRs abnormality remained unsolved, though it has been said not to produce ABRs abnormality. Among 8 cases under barbiturate therapy, there were 5 cases with no identifiable waves and 3 cases with 1st and 2 nd waves.(ABSTRACT TRUNCATED AT 250 WORDS)
The brain stem is an uncommon site of a brain abscess. Such lesions were invariably fatal before 1974, when the arrival of computed tomography and magnetic resonance imaging improved the prognosis. This new case with a good result shows the usefulness of early diagnosis, careful clinical and radiological monitoring and combined medical and surgical management. A child 2 1/2 years of age was admitted to the department of neurosurgery for diagnosis and treatment of a brain stem lesion. The clinical context and discovery of an intrabronchial foreign body, as well as neuroradiological investigations, suggested a diagnosis of brain stem abscess. Initial treatment with broad spectrum antibiotics with good cerebral penetration was associated with an increase in the size of the abscess and clinical worsening. Stereotactic aspiration of lesion was performed by a transpeduncular approach under CT guidance and general anaesthesia. Secondary thoracotomy enabled removal of an intrabronchial needle. After evacuation, in spite of failure to identify the organism, neurological deficit resolved rapidly and the lesion no longer appeared on CT. Management of a brain abscess always includes antibiotics. They must cover the organisms most often encountered in brain abscesses and have good cerebral penetration. Medical treatment seems to suffice for small abscesses. A brain stem abscess with rapid clinical signs, together with current neuroradiogical diagnostic techniques, enables early discovery of such abscesses when they are still small. Treatment of brain stem abscesses includes primary antibiotic therapy, then stereotaxic drainage when there is any diagnostic doubt, poor clinical tolerability or antibiotic resistance.
The brain stems from 52 corpses were microscopically examined. These cases died as a result of closed head injuries, which were clinically diagnosed and/or diagnosed postmortem as primary brain stem lesions. The morphological changes in these cases were compared with morphological changes in the brain stems of corpses who died from cerebral hemorrhage with additional secondary brain stem lesions. The examinations revealed acidophilic necrosis of the vessel walls in brain stem hemorrhages with fibrin impregnation of the vessel walls. Fibrin penetration to the perivascular space was the basic morphological marker that helped to differentiate between these two groups of cases.
To clarify the effects of disturbances in basilar artery blood flow, basilar artery angiospasm was induced in 2 cats and 4 guinea pigs and auditory brain-stem responses (ABRs) were continuously recorded preceding, during and following the angiospasm. The angiospasm caused specific ABR changes in that waves II (P2-N2) and III (P3-N3) were attenuated without any corresponding amplitude reduction of P4. Those changes were equivalent following stimulation of either ear. Moreover, the ABR changes gradually recovered within 5 h. On the basis of the animal experiments, 52 patients with subarachnoid hemorrhage, supratentorial tumor showing increased intracranial pressure or hydrocephalus were selected for repeated ABR examinations. ABR abnormalities similar to those observed in the animal experiment were obtained especially from the patients exhibiting grade 3 or 4 symptomatology with subarachnoid hemorrhage. In these cases, the wave III to wave IV-V amplitude ratio was significantly decreased. In some cases the ABR abnormalities and the wave III to wave IV-V amplitude ratio recovered as the clinical course improved. These results support the conclusion that specific ABR changes (wave III to wave IV-V amplitude ratio) reflect transient ischemic dysfunction of the midline portion of the brain-stem caused by disturbances of basilar artery blood flow.
OBJECTIVE: To explore dynamic changes in brain-stem auditory electrophysiology during the neonatal period in term infants after perinatal asphyxia. METHODS: Sixty-eight term newborn infants who suffered asphyxia were studied on days 1, 3, 5, 7, 14 and 30 after birth. Brain-stem auditory evoked response (BAER) was recorded with clicks, delivered at 21, 51 and 91 s(-1) and > or =40 dB above BAER threshold of each subject. RESULTS: During the neonatal period wave I latency in the infants after asphyxia increased slightly while later BAER components changed more significantly. On the first day after birth wave III and V latencies and I-V and III-V intervals increased significantly at all rates of clicks (ANOVA P<0.01-0.001). On day 3, the latencies and intervals increased further. III-V/I-III interval ratio increased at 51 and 91 s(-1), suggesting a relatively more significant increase in III-V interval than in I-III interval at higher rates. Thereafter, wave III and V latencies and all intervals decreased progressively, although these BAER variables were still significantly longer than in normal controls on days 5 and 7 (P<0.05-0.001) On day 30, all latencies and intervals approached near normal values, with a slight increase in wave V latency and I-V and III-V intervals at 51 and 91 s(-1). CONCLUSIONS: Perinatal asphyxia has a major effect on central auditory function, resulting in acute impairment. The impairment progresses during the first 3 days and then tends towards recovery. By 1 month the impaired auditory function has largely returned to normal. Significant increase in click rates can moderately improve the detection of auditory impairment. SIGNIFICANCE: After perinatal asphyxia early detection of hypoxic-ischaemic damage to the central auditory system and initialisation of neuroprotective and therapeutic measures during the first hours after birth are critical to prevent or reduce deterioration of central impairment.
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The brain stem is an unusual location for a pyogenic abscess. We report a case of a brain stem abscess in a 5-year-old boy with tetralogy of Fallot that was refractory to conservative medical therapy but was cured after a single computed tomographic-guided stereotactic aspiration and appropriate antibiotic therapy. The remarkable features in this case were the extremely large size of the abscess (3.2 cm in diameter), occupying the full vertical extent of the brain stem and containing 15 ml of pus. We believe this is the first report of a favorable outcome in a cardiogenic brain stem abscess. The value of computed tomographic-guided stereotactic surgery in the management of this lethal condition is documented with a review of the relevant literature.
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OBJECTIVES: We evaluated comatose patients by auditory brain stem responses (ABR) to determine the role of ABR in the diagnosis of impending brain death. PATIENTS AND METHODS: Sixty comatose patients in the intensive care unit were evaluated by brain stem evoked response audiometry. Correlations were sought between the absence or presence of ABRs and the presenting pathology, the Glasgow Coma Scale (GCS) scores, and ultimate diagnoses. RESULTS: The brain stem responses were totally absent in 41 patients. Presence of wave I could be obtained in only 10 patients. All the waveforms were found in nine patients; however, in eight patients the potentials disappeared as the GCS scores decreased to 3. Detection of wave I alone strongly suggested dysfunction of the brain stem. However, loss of wave I particularly in trauma patients aroused doubt as to whether the absence was associated with auditory end organ injury or brain stem dysfunction. CONCLUSION: The results suggest that evaluation of ABR may support brain death in a comatose patient (i) when wave I is present alone, (ii) the absence of wave I is accompanied by a documented auditory end organ injury, or (iii) when previously recorded potentials are no longer detectable.
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Patients with various forms of cerebral circulation impairment were examined. The changes of evoked truncal acoustic potentials (ETAP) point to a lesion of the brain stem formations predominantly at a mesencephalic level. It has been shown that ETAP correlate with the neurological symptomatology.
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