1/82. Analysis of the perception of and reactivity to pain and heat in patients with wallenberg syndrome and severe spinothalamic tract dysfunction. BACKGROUND: The aim of the study was to assess the consequences of severe spinothalamic tract lesions resulting from lateral medullary infarct and to show that a specific pain perception can be elicited by strong thermal stimulation. CASE DESCRIPTIONS: Both patients examined presented with severe thermoalgic dissociation of the limbs contralateral to the lesion, with normal discriminative somatosensory perception and motor strength. They reported pain perception when touching very warm (>50 degrees C to 60 degrees C) objects and a brisk, occasionally uncontrolled withdrawal reaction of the arm and hand under the same conditions, without any perception of the heat nature of the stimulus. Warm stimulation, <45 degrees C, elicited no thermal perception or discrimination. pain perception could be elicited in both patients by increasing the temperature, with a reproducible threshold of 47 degrees C to 49 degrees C. Pain always occurred after a prolonged delay of 8 to 10 seconds in response to threshold heat, and was described as deep and osseous, and clearly different from that perceived on the nonaffected side. The delay was much shorter when the temperature was increased by 4 degrees C to 5 degrees C. Cold stimulation elicited similar pain perception in one patient. Analysis of subjective perception of laser stimulation showed a much higher pain threshold on the affected hand. There were no laser-evoked potentials on this side, which suggested major spinothalamic injury. Assessment of the RIII noxious reflex revealed persistent response withdrawal reactions, with an increased threshold on the affected side, and partial consciousness of the noxious nature of the stimulus. CONCLUSIONS: To our knowledge, this is the first description of the appearance of pain perception of high temperatures in patients with severe spinothalamic injury who are suffering from a complete loss of temperature perception. This implies that noxious thermal stimulation can still be perceived via extra spinothalamic pathways (which are slow and multisynaptic), such as the spinoreticulothalamic tract. patients with Wallenberg syndrome should be informed and made aware of their residual perception of and reactions to noxious stimulation. ( info) |
| Four consecutive patients with lateral medullary syndrome reported reversible inability to complete a reflex sneeze, despite retaining the urge to do so and the ability to mimic the motor act. This previously undescribed feature of a relatively common syndrome is in keeping with the known location of a "sneeze center" in the lateral medulla of cat. In man, unilateral brainstem lesion is sufficient to abolish the sneeze reflex temporarily. ( info) |
3/82. Posterior fossa arteriovenous malformation associated with persistent primitive trigeminal artery--case report. A 21-year-old female presented with an unusual case of posterior fossa arteriovenous malformation (AVM) associated with ipsilateral persistent primitive trigeminal artery (PPTA), manifesting as intraparenchymal hemorrhage involving both the brain stem and the left cerebellar hemisphere. The presenting symptoms were compatible with Wallenberg's syndrome and Foville's syndrome on the left side. She was initially treated conservatively, and subsequently with transarterial embolization followed by stereotactic radiosurgery. This case combined the rare association of posterior fossa AVM and PPTA, with the clinical presentation of intraparenchymal hemorrhage causing both Wallenberg's syndrome and Foville's syndrome. ( info) |
| BACKGROUND: Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis. CASE DESCRIPTION: We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, <3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms(2), respectively; normal level, 0.14 /-0.02 ms(2)). MNSA was increased in frequency (61 bursts per minute; normal level, 34 /-18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact. CONCLUSIONS: Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunction, increased sympathetic activity, and neurogenic paroxysmal hypertension. ( info) |
5/82. Infarct presenting with a combination of Wallenberg and posterior spinal artery syndromes. This is the first report of a patient presenting with a combination of Wallenberg and posterior spinal artery syndromes. The patient developed right hemiplegia and sensory disturbances on the right side of the face and over the whole body. MRI showed infarcts of the cerebellum, medulla oblongata, and upper cervical cord. These lesions were in the territory of the right posterior inferior cerebellar artery (pica) and the right posterior spinal artery (PSA). The combination was due to severe stenosis of the right vertebral artery. ( info) |
6/82. Dissecting aneurysms of the posterior inferior cerebellar artery: report of four cases and review of the literature. Dissecting aneurysms frequently involve the vertebral arteries and their branches, but those exclusively on the posterior inferior cerebellar artery (pica) represent only 24 cases in the literature, including the four cases discussed in this article. The clinical diagnosis lacks pathognomonic signs or symptoms, with presentations such as subarachnoid haemorrhage or ischaemia of the brain stem or the cerebellum, and the management is controversial. Wrapping, clipping and embolisation of the aneurysms were tried in this series with different outcomes. Exclusion of the pathological segment should be performed, as shown by rebleeding from our case which was wrapped or by progression of the vascular disease in cases where treatment was delayed. Surgical or endovascular occlusion are well tolerated in our cases and in those reported from the literature, which implies the absence of normal perforating branches to the brain stem arising from the proximal dissected segment of the pica and a good collateral circulation. A revascularisation procedure using the occipital artery can be performed in order to prevent infarction if an endovascular test occlusion is not tolerated. ( info) |
7/82. vertigo and gait ataxia without usual signs of lateral medullary infarction: a clinical variant related to rostral-dorsolateral lesions. Isolated vertigo and ataxia have not been reported as manifestations of lateral medullary infarction. The author describes 3 patients with lateral medullary infarction who presented with almost isolated vertigo and gait ataxia without usual signs/symptoms of lateral medullary infarction such as facial/hemibody sensory changes, dysphagia, hoarseness, hiccup, limb ataxia, and Horner sign. Brain MRI showed small infarcts selectively involving the most dorsolateral portion of the rostral medulla that corresponds to the vestibulocerebellar pathway. These patients illustrate that lateral medullary infarction may present as an isolated vertigo and gait ataxia. Clinicians should be aware of this clinical variant, because these patients may be misdiagnosed as having labyrinthine disorders. ( info) |
8/82. Unusual occipital condyle fracture with multiple nerve palsies and Wallenberg syndrome. A 52-year-old male presented with an extremely rare fracture of the occipital condyle involving the jugular foramen with marked medial rostrad displacement of the fragments. He had ipsilateral VII through XII nerves palsies and Wallenberg syndrome. Conservative treatment did not improve the cranial nerve palsies. A high-resolution CT-scan is essential to visualize these fractures. ( info) |
9/82. Lateral medullary infarct presenting as acute dysphagia. Lateral medullary infarct (LMI) usually presents with a variety of neurological features. We describe a case of LMI in which acute dysphagia was the only initial symptom. This typical neurological syndrome is very unlikely to be found during ENT practice; however, it needs to be considered among the differential diagnoses when encountering dysphagia of uncertain origin. ( info) |
10/82. Dysphagia in a patient with lateral medullary syndrome: insight into the central control of swallowing. BACKGROUND & AIMS: Central control of swallowing is regulated by a central pattern generator (CPG) positioned dorsally in the solitary tract nucleus and neighboring medullary reticular formation. The CPG serially activates the cranial nerve motor neurons, including the nucleus ambiguus and vagal dorsal motor nucleus, which then innervate the muscles of deglutition. This case provides insight into the central control of swallowing. methods: A 65-year-old man with a right superior lateral medullary syndrome presented with a constellation of symptoms, including dysphagia. The swallow was characterized using videofluoroscopy and esophageal motility and the results were compared with magnetic resonance imaging (MRI) findings. RESULTS: Videofluoroscopy showed intact lingual propulsion and volitional movements of the larynx. Distal pharyngeal peristalsis was absent, and the bolus did not pass the upper esophageal sphincter. manometry showed proximal pharyngeal contraction and normal peristaltic activity in the lower esophagus (smooth muscle), but motor activity of the upper esophageal sphincter and proximal esophagus (striated muscle) was absent. MRI showed a lesion of the dorsal medulla. CONCLUSIONS: These findings are compatible with a specific lesion of the connections from a programming CPG in the solitary tract nucleus to nucleus ambiguus neurons, which supply the distal pharynx, upper esophageal sphincter, and proximal esophagus. There is functional preservation of the CPG control center in the solitary tract nucleus and of the vagal dorsal motor nucleus neurons innervating the smooth muscle esophagus. ( info) |