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Detection of apoptosis in human brainstem by TUNEL assay.

The aim of the present study was to evaluate the distribution of apoptotic neurons in the nuclei of the brainstem. Apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay, in human brainstems taken at autopsy from 15 adults (age range: 25-58 years). The nuclei examined included the hypoglossal nucleus (XII), dorsal motor nucleus of the vagus (DMNV), solitary tract nucleus (STN), vestibular nucleus (Ve), cuneate nucleus (Cu), nucleus of the spinal trigeminal tract (NSTT), principal inferior olivary nucleus (PION), medial inferior olivary nucleus (MION) and dorsal inferior olivary nucleus (DION). For each nucleus, the apoptotic index was expressed as the percentage of TUNEL-positive neurons out of the total number of neurons counted. Statistical analysis was performed with one-way ANOVA and Student-Newman-Keuls test for multiple comparisons. One-way ANOVA revealed that the differences in apoptotic index among the nuclei were statistically significant (P<0.001). Cu had the highest index, corresponding to 29.5 +/- 14.2%. The Student-Newman-Keuls test revealed significant differences when this value was compared with those of XII (14.1 +/- 12.0%; P<0.05), PION (12.8 +/- 13.8%; P<0.01), DION (12.0 +/-12.4%; P<0.01), MION (12.0 +/- 15.7%; P<0.01), STN (8.5 +/- 11.9%; P<0.001) and DMNV (5.4 +/- 6.8%; P<0.001). The differences in apoptotic index between Cu and NSTT (27.1 +/- 18.1%) and between Cu and Ve (23.7 +/- 12.6%) were not statistically significant (P>0.05). The apoptotic index in the NSTT was higher than in DMNV (P<0.001), STN (P<0.01) and nuclei of the inferior olivary complex (P<0.05). Ve showed a higher apoptotic index with respect to DMNV (P<0.01) and STN (P<0.05). Apoptotic processes found in the brainstems were ascribed to hypoxic-ischemic injury, and heterogeneity in apoptotic index among the nuclei supports the hypothesis of the differing vulnerability of the nuclei of the brainstem.

Adult↗

Course and distribution of facial corticobulbar tract fibres in the lower brain stem.

The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus.

Adult↗

[Imaging techniques in diagnosis of brainstem infarction].

Twenty per cent of cerebral ischaemic infarctions involve tissue, supplied by the vertebrobasilar circulation. This overview of the current literature and our own experiences present the value of different imaging techniques (CT and MRI) and new developments for diagnosing brainstem infarction. Furthermore, the roles of invasive and noninvasive vascular imaging methods (computed tomographic angiography, magnetic resonance angiography, intra-arterial angiography, ultrasound) for evaluating vertebrobasilar stenosis and occlusion are described. The diagnostic workup of the most severe form of brainstem infarction, basilar artery thrombosis, is shown.

Brain Stem Infarctions↗

Bilateral Wallerian degeneration of the middle cerebellar peduncles due to paramedian pontine infarction: MRI findings.

Wallerian degeneration is a frequent finding in lesions of the pyramidal tract, but has been observed after damage of the other fibre systems as well. Few reports exist about Wallerian degeneration of cerebellar fibres after distant lesions to the axons. Here, we report on a patient who developed degeneration of both middle cerebellar peduncles after a paramedian pontine infarction.

Aged↗

Bilateral medial medullary infarction.

We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid.A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated.

Aged↗

Bilateral medial medullary infarction due to bilateral vertebral artery dissection.

We describe a 52-year-old woman who experienced transient motor weakness and numbness of the left extremities and presented 2 days later with severe hemiparesis and sensory impairment of the right extremities and right lingual palsy. Magnetic resonance imaging (MRI) revealed bilateral upper medial medullary infarction, primarily in the left ventral portion. The findings of both three-dimensional (3D) computed tomographic and conventional angiography suggested dissection of both intracranial vertebral arteries (VAs). Medial medullary infarction is generally caused by atherosclerosis within a VA or anterior spinal artery. This is the first report of bilateral medial medullary infarction due to dissection of both intracranial VAs.

Brain Stem Infarctions↗