Effect of Transcutaneous Vagus Nerve Stimulation in Dysphagia After Lateral Medullary Infarction: A Case Report.

Purpose Severe dysphagia with weak pharyngeal peristalsis after dorsal lateral medullary infarction (LMI) requires long-term tube feeding. However, no study is currently available on therapeutic effectiveness in severe dysphagia caused by nuclear damage of vagus nerve after dorsal LMI. The purpose of the present investigation was to explore the potential of transcutaneous vagus nerve stimulation (tVNS) to improve severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Method We assessed the efficacy of 6-week tVNS in a 28-year-old woman presented with persisting severe dysphagia after dorsal LMI who had been on nasogastric feeding for 6 months. tVNS was applied for 20 min twice a day, 5 days a week, for 6 weeks. The outcome measures included saliva spitted, Swallow Function Scoring System, Functional Oral Intake Scale, Clinical Assessment of Dysphagia With Wallenberg Syndrome, Yale Pharyngeal Residue Severity Rating Scale, and upper esophagus X-ray examination. Results After tVNS, the patient was advanced to a full oral diet without head rotation or spitting. No saliva residue was found in the valleculae and pyriform sinuses. Contrast medium freely passed through the upper esophageal sphincter. Conclusion Our findings suggest that tVNS might provide a useful means for recovery of severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Supplemental Material https://doi.org/10.23641/asha.9755438.

Unusual neurological syndrome induced by atmospheric pressure change.

BACKGROUND: We describe a case of a 46-yr-old female who developed hypertension, tachycardia, dysarthria, and leg weakness provoked by pressure changes associated with flying. Typically during the landing phase of flight, she would feel dizzy and note that she had difficulty with speech and leg weakness. After the flight the leg weakness persisted for several days. The symptoms were mitigated when she took a combined alpha-beta blocker (labetalol) prior to the flight. CASE STUDY: To determine if these symptoms were related to atmospheric pressure change, she was referred for testing in a hyperbaric chamber. She was exposed to elevated atmospheric pressure (maximum 1.2 ATA) while her heart rate and blood pressure were monitored. Within 1 min she developed tachycardia and hypertension. She also quickly developed slurred speech, left arm and leg weakness, and sensory changes in her left leg. She was returned to sea level pressure and her symptoms gradually improved. A full neurological workup has revealed no explanation for these findings. She has no air collections, cysts, or other anatomic findings that could be sensitive to atmospheric pressure change. DISCUSSION: The pattern is most consistent with a vascular event stimulated by altitude exposure. This case suggests that atmospheric pressure change can produce neurological symptoms, although the mechanism is unknown.

Ondine's curse with accompanying trigeminal and glossopharyngeal neuralgia secondary to medullary telangiectasia.

BACKGROUND: Central hypoventilation syndrome ("Ondine's Curse") is an infrequent disorder that can lead to serious acute or chronic health consequences. This syndrome, especially in adults, is rare, and even less frequent in the absence of clear pathogenic lesions on MRI. In addition, we are not aware of any previously reported cases with associated cranial nerve neuralgias. METHODS: We describe a patient with baseline trigeminal and glossopharyngeal neuralgia, admitted with episodes of severe hypoventilatory failure of central origin, consistent with "Ondine's Curse". After evaluation, she was found to have a medullary capillary telangiectasia, thought to be the causative lesion, and which could explain her complete neurologic and hypoventilatory syndrome. The patient was treated with placement of a diaphragmatic pacing system, which has been effective thus far. RESULTS: This case illustrates the need for investigation of centrally mediated apnea, especially when co-occurring cranial nerve neuralgia is present and cardiopulmonary evaluation is negative. It provides an example of capillary telangiectasia as the causative lesion, one that to our knowledge has not been reported before. CONCLUSIONS: Placement of a diaphragmatic pacing system was warranted and became lifesaving as the patient was deemed to be severely incapacitated by chronic ventilatory insufficiency.

Recovery of reversed basilar artery flow as seen by transcranial sonography and MRA source images for vertebral dissection.

The dissection of the intracranial vertebral artery (VAD) is a common cause of young age brain stem stroke. VAD can be detected by conventional angiography, but there is yet no agreement on the most effective tool to use for the detection of VAD. Here, we report a patient with VAD, who was diagnosed with an intimal flap within the left vertebral artery by the magnetic resonance angiography (MRA) source images. Transcranial Doppler (TCD) showed a reversed flow in the basilar artery. After 4 months, TCD and transcranial color-coded Doppler (TCCD) confirmed a normal anterograde flow of the vertebro-basilar arteries.

[Morphometric characteristic of some structures of the human brain in normal conditions and in acute ethanol intoxication]. / Morfometricheskaia kharakteristika struktur golovnogo mozga cheloveka v norme i v usloviiakh ostroi intoksikatsii étanolom.

In order to establish the neuro-stromal interrelations in the human brain under normal conditions and after extreme influences, different parts of this organ were studied in 14 persons who died suddenly and in 20 persons who died of ethyl alcohol poisoning. A complex of histological, histochemical, planimetric and morphometric methods were used. The specific area of normal neurocytes was shown to be the largest in the medulla oblongata, while that one of the fibers--in the cerebral cortex. Vascularization of the latter is minimal, being much higher in the medulla oblongata. In alcohol intoxication, the area, occupied by neurocytes, was decreased in the cerebral cortex, thalamus and cerebellum due to the destruction of some portion of these cells. In the medulla oblongata neurocytes appear to be more resistant to ethanol. The capillary diameter in the brain areas studied decreased because of the drop in the tone of cerebral arteries, but the number of these vessels per standard area of section was increased as a result of compensatory opening of reserve capillaries.

[The medial medullary infarction (Dejerine syndrome) following chiropractic neck manipulation].

A-38-year-old man suddenly developed nausea, vomiting and vertigo during chiropractic neck manipulation. This was followed by right hemiplegia, right deep sensory disturbance and left hypoglossal nerve palsy, consistent with the medial medullary infarction (Dejerine syndrome). The MRI revealed infarction at left medial part of the medulla. The vertebral angiogram and MRA showed marked narrowing of the left vertebral artery. X-rays of the cervical spine showed no spondylosis, dislocation nor osteolysis of the odontoid process. The serological studies, including lupus anticoagulant, protein C, and protein S gave normal results. Although vascular accidents involving the brain stem after chiropractic neck manipulation have been reported since Pratt-Thomas and Berger, previous reports are still rare. In them lateral medullary infarction (Wallenberg syndrome) is probably the most common case. On the other hand, medial medullary syndrome (Dejerine syndrome) is absolutely rare. To our knowledge, the only one report has been made by Watanabe and his colleagues before our present case. The mechanism was suggested that rotation and tilting of the neck stretches and compresses the vertebral artery at the cervical joint causing injury to the vessel, with an intimal tearing, dissection, and pseudoaneurysm formation. Consequently, the present case may be caused by injury to the left vertebral artery with an intimal tearing during neck manipulation sufficient to cause disection and subsequent infarction of the brain stem.

MRI characteristics of acute and subacute brainstem and thalamic infarctions: value of T2- and diffusion-weighted sequences.

MRI including diffusion-weighted sequences (DW-MRI) has demonstrated its high sensitivity for acute supratentorial ischemic lesions. In this study we examined the sensitivity of different MRI sequences for the detection of acute brainstem and isolated thalamic infarctions. Diffusion- and T2-weighted MRI of 45 consecutive patients with signs and symptoms of infratentorial and thalamic infarction between 6/1997 and 1/2000 were analysed. The time between the onset of symptoms and the first MRI varied between 2 hours to 7 days with a median of 2 days. MRI repeats were performed in 4 patients in whom the clinical brainstem infarction had not been detected initially. Lesion detectability and size were evaluated for different brainstem and thalamic localizations. An acute brainstem or thalamic infarction as defined by the clinical condition could be identified in all patients by comparison of DW-MRI and T2-weighted images. Pons in farctions were the largest, followed by midbrain and thalamic lesions. Medulla oblongata infarctions were small in comparison. Pons, mid-brain and thalamic infarctions were reliably identified beginning 12 hours after the onset of symptoms. In contrast, detectability of medulla oblongata infarctions varied within the first 24 hours and their overall visibility was worse than that of other brainstem infarctions corresponding to their small size. However, regardless of loca tion, none of the 3 infarctions examined within the first 5 hours after the onset of symptoms could be identified. These lesions were demonstrated in follow-up examinations. In conclusion, pontine, midbrain and thalamic infarctions can reliably be visualized by a combination of DW-MRI and T2-weighted images beginning 12 hours after the ischemic attack. However, sensitivity seems to be lower earlier than 12 hours after ischemia and for medulla oblongata lesions.

Noradrenaline synthesis, release and vesicular transport in the rat brain following subarachnoid haemorrhage.

The present study was designed to estimate the release of noradrenaline, and to evaluate the efficiency of noradrenaline vesicular transport, as indicated from measures of dihydroxyphenylglycol (DHPG), and synthesis in the medulla and hypothalamus following subarachnoid haemorrhage in rats. Subarachnoid haemorrhage was induced by the injection of homologous blood into the cisterna magna (n = 11). Sham operated animals served as controls (n = 11). Three days following subarachnoid haemorrhage, medulla and hypothalamus were dissected and placed in an in vitro superfusion system. Exposure to K(+) (50 mM) for 2 min served as a stimulus for the release of the neurotransmitter noradrenaline, its precursor (dihydroxyphenylalanine [DOPA]) and intraneuronal metabolite, DHPG. Basal noradrenaline overflow from both the medulla and hypothalamus were similar in the two groups of rats but basal DOPA overflow from the medulla was significantly reduced in the subarachnoid haemorrhage animals (0.97 +/- 0.15 vs. 1.97 +/- 0.38 pg/10 min/mg, p < 0.01). Administration of K(+) induced the release of noradrenaline, the response from the medulla in the subarachnoid haemorrhage group being attenuated (p < 0.01) compared with the sham operated animals (174% and 240%, respectively). K(+) induced a similar release of noradrenaline from the hypothalamus in both groups of rats (239% in sham animals and 283% in the subarachnoid haemorrhage group). The overflow of DHPG from both the hypothalamus and medulla was similar in both groups of animals. Our results suggest that the diminution in noradrenaline release from the medulla occurs as a result of a reduction in the rate of noradrenaline synthesis and release.

Deformation of the ventrolateral medulla oblongata by subarachnoid hemorrhage from ruptured vertebral artery aneurysms causes neurogenic pulmonary edema.

The occurrence of neurogenic pulmonary edema (NPE) associated with subarachnoid hemorrhage (SAH) due to ruptured aneurysm was analyzed in 48 consecutive patients. Correlations of the location of the aneurysm, clinical grade, amount of subarachnoid clot, and severity of NPE were examined. NPE was observed in 29.4% of all SAH cases, but the incidence was significantly higher in cases of ruptured vertebral artery (VA) aneurysm. Clinical grade, severity of NPE, and deformation of the medulla oblongata were studied in the five cases of ruptured VA aneurysm. Deformation of the ventrolateral medulla oblongata was observed in all patients. Asymmetry index of the medulla oblongata measured on the axial computed tomography scan was correlated with the severity of NPE. Severity of NPE tended to correlate with deformation of the medulla oblongata. NPE associated with ruptured VA aneurysm is caused by deformation of the ventrolateral site of the medulla oblongata by the localized hemorrhage.

Cavernous malformations of the brainstem: experience with 100 patients.

OBJECT: In this study the authors review surgical experience with cavernous malformations of the brainstem (CMBs) in an attempt to define more clearly the natural history, indications, and risks of surgical management of these lesions. METHODS: The authors retrospectively reviewed the cases of 100 patients (38 males and 62 females; mean age 37 years) harboring 103 lesions at treated a single institution between 1984 and 1997. Clinical histories, radiographs, pathology records, and operative reports were evaluated. The brainstem lesions were distributed as follows: pons in 39 patients, medulla in 16, midbrain in 16, pontomesencephalic junction in 15, pontomedullary junction in 10, midbrain-hypothalamus/thalamus region in two patients, and more than two brainstem levels in five. The retrospective annual hemorrhage rate was most conservatively estimated at 5% per lesion per year. Standard skull base approaches were used to resect lesions in 86 of the 100 patients. Intraoperatively, all 86 patients were found to have a venous anomaly in association with the CMB. Follow up was available in 98% (84 of 86) of the surgical patients. Of these, 73 (87%) were the same or better after surgical intervention, eight (10%) were worse, and three (4%) died. Two surgical patients were lost to follow-up review. Incidences of permanent or severe morbidity occurred in 10 (12%) of the surgically treated patients. The average postoperative Glasgow Outcome Scale score for surgically treated patients was 4.5, with a mean follow-up period of 35 months. CONCLUSIONS: The natural history of CMBs is worse than that of cavernous malformations in other locations. These CMBs can be resected using skull base approaches, which should be considered in patients with symptomatic hemorrhage who harbor lesions that approach the pial surface. Venous anomalies are always associated with CMBs and must be preserved.

Iatrogenic Wernicke's encephalopathy in allogeneic bone marrow transplantation: a study of eight cases.

Wernicke's encephalopathy (WE) is a neuropsychiatric condition generally caused by acute thiamine deficiency and classically involves the triad of altered mentation, ataxia and ophthalmoplegia. It is most common among alcoholics, but several other causes have been identified, including total parenteral nutrition (TPN) use. We present eight cases of WE in patients undergoing allogeneic BMT, where thiamine deficiency was caused by a lack of vitamin supplementation during TPN administration. Clinically, WE presented as a severe refractory metabolic acidosis, preceded by 'raspberry tongue', and ophthalmologic and neurologic dysfunction. The sites most affected were the periventricular structures and the thalamus, and no mammilary bodies lesions were found.

[Medial medullary infarction following neck manipulation].

Reported is a case of a 39-year-old man with medial medullary infarction following chiropractic neck manipulation. Neurologically, he showed right hemiparesis sparing the face, right deep sensory impairment and tongue deviation to the left in five hours after neck manipulation. A cranial MRI revealed an ischemic lesion in the left medial portion of the medulla oblongata. Cerebral angiography demonstrated no apparent organic lesion of the right vertebral artery (VA), but showed hypoplasia of the left VA. We suspect that the left medial medullary infarction occurred because of the reduced VA blood flow following the contralateral VA compression, in addition to the ipsilateral VA hypoplasia. This case is the first one reported in which medial medullary infarction was possibly induced by neck manipulation.

Effect of naloxone on regional cerebral blood flow during endotoxin shock in conscious rats.

Maintenance of cerebral blood flow (CBF) is vital during cardiovascular shock. Since opioids have been implicated in the pathophysiology of endotoxin shock and have been shown to alter cerebral perfusion patterns, we determined whether opioids were responsible for any of the changes in regional CBF observed during endotoxin shock and whether the use of naloxone might impair or aid in the maintenance of CBF. When blood flow (BF) is studied with microspheres in rats, the left ventricle of the heart is often cannulated via the right carotid artery. Questions have arisen concerning the potential adverse effects of this method on CBF in the hemisphere ipsilateral to the ligated artery. We measured right and left regional CBF by use of this route of cannulation. Twenty-four hours after cannulations were performed, flow measurements were made using radiolabeled microspheres in conscious unrestrained male Sprague-Dawley rats (300-400 g) before and 10, 30 and 60 min after challenging with 10 mg/kg Escherichia coli endotoxin (etx) or saline. Naloxone (2 mg/kg) or saline was given as a treatment 25 min post-etx. We found no significant differences between right and left cortical, midbrain, or cerebellar BF at any time in any treatment group. After etx, the whole brain received a large share of the depressed cardiac output. Thus global CBF was not significantly reduced below its pre-etx value, an effect unaltered by naloxone. Regionally, BF was reduced to cerebellum and midbrain by 30 min post-etx. Naloxone prevented this depression. No region was affected to a greater or lesser degree than others.(ABSTRACT TRUNCATED AT 250 WORDS)

[Morphofunctional changes in the adrenergic innervation of the major cerebral arteries during bilateral electrostimulation of the locus coeruleus]. / Morfofunktsional'nye izmeneniia adrenergicheskoi innervatsii magistral'nykh arterii mozga pri bilateral'noi élektrostimuliatsii golubogo piatna.

The intramural adrenergic nervous apparatus of cerebral arteries was studied in adult rabbits after 3-10 sessions of electrical stimulation of locus coeruleus. The activity of nerve structures was determined by estimating the density of adrenergic perivascular plexuses and by semi-quantitative cytophotometry of changes in the catecholamine content of nerve varicosities. The stimulation was followed by a 28.2 +/- 1.5% increase in adrenergic innervation density. while catecholamine content in perivascular nerve structures displayed a tendency to decrease. The problem of central effects on cerebral blood flow autoregulation is discussed.

Effect of hemorrhage on regional morphometric indexes of cerebral capillarity.

This study was performed to determine whether the brain can increase the number of perfused capillaries and arterioles supplying it regionally during hemorrhage. This was done using a technique to simultaneously determine total and perfused regional arteriolar and capillary morphology. Conscious Long-Evans rats served as unbled controls or were bled 65 mmHg or to 40-45 mmHg and stabilized for 30 min. Regional cerebral blood flow was determined using [14C]iodoantipyrine in half of these animals and fluorescein isothiocyanate-dextran was injected in the other half for determination of perfused cerebral microvascular morphometric indexes. The total microvasculature was labeled postmortem via an alkaline phosphatase stain. Regional cerebral blood flow was significantly increased in animals bled to 65 mmHg. During hemorrhage to 40-45 mmHg, cerebral blood flow was reduced 50% (from 59 +/- 28 to 26 +/- 11 ml X min-1 X 100 g-1, mean +/- SD) with no regional redistribution. For all treatments, total capillary density ranged from 400 to 500 capillaries/mm2, and in controls 47% were perfused. Animals bled to 65 mmHg did not mobilize their unperfused microvascular reserve even though they showed a slight tendency to do so. During hemorrhage to 40-45 mmHg, this percent increased significantly to 57% with the largest increase occurring in the pons. Approximately 51% of arterioles were perfused in controls and this was not different compared with the percent perfused during hemorrhage. Despite the overall lack of mobilization of unperfused arterioles, some regions within the brain significantly mobilized their reserves with severe hemorrhage, e.g., hippocampus (78%), hypothalamus (67%), and medulla (73%).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of acute and chronic morphine on regional distribution of cardiac output in brain.

Both acute and chronic administration of morphine resulted in an increase in the percent cardiac output received by brain. However, various brain regions were affected differently by the drug treatments. The greatest increases in percent cardiac output received after chronic administration of morphine occurred in pons and cerebellum, while the greatest increases after acute administration occurred in cortex and midbrain. The changes found are in contrast with earlier studies which suggest that morphine has no effect on cerebral blood flow.

Role of computed tomography in vertebrobasilar ischemia.

Precise delineation of vertebrobasilar ischemia by computed tomography (CT) appears difficult due to the numerous variations in distribution of the posterior fossa arterial supply. While pontine and upper brainstem infarctions can be readily demonstrated, medullary infarction remains beyond the scope of present CT scanners. CT findings in cases of basilar artery occlusion include bilateral pontine infarction or extensive brainstem ischemia, associated with cerebellar and posterior cerebral vascular damage. Demonstration of basilar artery occlusion using routine CT is only rarely achieved. In cerebellar ischemia, CT, in conjunction with clinical syndromes, helps in the recognition of the arterial territory involved. CT provides useful guidelines for the treatment of cerebellar stroke, leading to surgery in cases of massive cerebellar infarction.

Total and regional cerebral blood flow during moderate and severe exercise in miniature swine.

To determine the influence of exercise on cerebral blood flow, we ran 14 swine at 3-6 mph and at 0-10% grades on a treadmill for 30 min at moderate and severe levels of exercise. Measuring heart rate, cardiac output, and aortic pressure via implanted probes, we injected 15-mum radiolabeled microspheres via the left atrium before and during exercise. We measured their distribution by gamma spectrometry, determining total cerebral blood flow, regional blood flow, and ratio of flow to gray and white matter. Heart rate, cardiac output, and aortic pressure rose progressively with increasing exercise. Total cerebral flow resembled that reported in humans, i.e., it did not change significantly with exercise. Regional flow distribution also failed to change significantly with exercise. The ratio of gray to white matter flow did not change except to the cerebellum where it rose significantly from resting values at both moderate and severe exercise. Gray matter received more flow than white matter during all three conditions of observation. Cerebral blood flow was remarkably constant during even severe exercise.

[Measurement of the blood flow in various areas of the rat brain by means of microspheres]. / Mesure du flux sanguin dans les différentes régions du cerveau du rat au moyen de microsphères

A method is described to measure regional blood flow in different structures of the rat brain. Microspheres (15 micron) are injected, the brain is sectioned, stained for myeline, radioautographs are prepared and the microspheres in the different structures are counted. The values obtained for different brain structures are counted. The values obtained for different brain regions (cortex, corpus callosum, thalamus hipocampus, hypothalamic region, colliculi, cerebellum, pons, medulla) compare well with those published by others on larger animals. In rats fed 1% of lead from birth, higher blood flow is found in the cortex and a lower one in the interior part of the brain compared to controls.