Analysis of the perception of and reactivity to pain and heat in patients with wallenberg syndrome and severe spinothalamic tract dysfunction.
(1/40)
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)
Blink reflex R2 changes and localisation of lesions in the lower brainstem (Wallenberg's syndrome): an electrophysiological and MRI study.
(2/40)
OBJECTIVES: Pathways of late blink reflexes are detected by high resolution MRI. Electronically matched stroke lesions superimposed to an anatomical atlas show the suspected course. METHODS: Fifteen patients with infarction of the lower brainstem, MRI lesions and electrically elicited blink reflexes were examined. The involved structures in patients with R2 and R2c blink reflex changes were identified by biplane high resolution MRI with individual slices matched to an anatomical atlas at 10 different levels using digital postprocessing methods. RESULTS: The blink reflexes were normal in five of 15 patients (33%) and showed loss or delay of R2 and R2c to stimulation ipsilaterally to lesion (R2-i and R2c-i) in eight (53%). Loss or delay of R2-i/R2c-i was seen in lesions covering the entire trigeminal spinal tract and nucleus (TSTN) at at least one level. These infarctions were located more dorsally within the medulla. Patients with normal blink reflexes showed lesions sparing or involving the TSTN only partially. They more often had incomplete Wallenberg's syndromes and MRI lesions were located more ventrally. CONCLUSIONS: Using digital postprocessing MRI methods it was possible to identify central pathways of late blink reflex in patients with Wallenberg's syndrome. This method is suggested as a new approach to identify incompletely understood functional structures of the brainstem. (+info)
Sensory sequelae of medullary infarction: differences between lateral and medial medullary syndrome.
(3/40)
BACKGROUND AND PURPOSE: A comparison between long-term sensory sequelae of lateral medullary infarction (LMI) and medial medullary infarction (MMI) has never been made. METHODS: We studied 55 patients with medullary infarction (41 with LMI and 14 with MMI) who were followed up for >6 months. We examined and interviewed the patients with the use of a structured format regarding the most important complaints, functional disabilities, and the presence of sensory symptoms. The nature and the intensity of sensory symptoms were assessed with the modified McGill-Melzack Pain Questionnaire and the visual analog scale, respectively. RESULTS: There were 43 men and 12 women, with an average age of 59 years. Mean follow-up period was 21 months. The sensory symptoms were the most important residual sequelae in LMI patients and the second most important in MMI patients. In LMI patients, the severity of residual sensory symptoms was significantly related to the initial severity of objective sensory deficits (P<0.05). Sensory symptoms were most often described by LMI patients as numbness (39%), burning (35%), and cold (22%) in the face, and cold (38%), numbness (29%), and burning (27%) in the body/limbs, whereas they were described as numbness (60%), squeezing (30%) and cold (10%), but never as burning, in their body/limbs by MMI patients. LMI patients significantly (P<0.05) more often cited a cold environment as an aggravating factor for the sensory symptoms than did the MMI patients without spinothalamic sensory impairment. The subjective sensory symptoms were frequently of a delayed onset (up to 6 months) in LMI patients, whereas they usually started immediately after the onset in MMI patients. CONCLUSIONS: Our study shows that sensory symptoms are major sequelae in both LMI and MMI patients. However, the nature, the mode of onset, and aggravating factors are different between the 2 groups, which probably is related to a selective involvement of the spinothalamic tract by the former and the medial lemniscus by the latter. We suggest that the mechanisms for the central poststroke pain or paresthesia may differ according to the site of damages on the sensory tracts (spinothalamic tract versus medial lemniscal tract). (+info)
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)
Brain stem stroke causing baroreflex failure and paroxysmal hypertension.
(5/40)
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)
Dysphagia in lateral medullary infarction (Wallenberg's syndrome): an acute disconnection syndrome in premotor neurons related to swallowing activity?
(6/40)
BACKGROUND AND PURPOSE: We have investigated the pathophysiological mechanisms of dysphagia in Wallenberg's syndrome (WS) that are due to lateral medullary infarction (LMI). METHODS: Twenty patients with WS were evaluated by means of clinical and electrophysiological methods that measured the oropharyngeal phase of voluntarily initiated swallowing. For comparison, 22 patients with unilateral hemispheric infarction were investigated during the acute stage of stroke, and 4 patients with unilateral peripheral 9th and 10th cranial nerve palsies were studied. Age-matched 30 healthy control subjects were also included in the study. RESULTS: It was found that dysphagia was clinically more severe in WS patients than in the patients in the other groups. The pharyngeal phase of swallowing was predominantly impaired, whereas in patients with hemispheric stroke, dysphagia was related only to the delay of triggering of the voluntarily induced swallowing. In WS patients, the swallowing reflex was extremely slow in spite of the unilateral involvement due to LMI, whereas the pharyngeal phase of reflex swallowing remained within normal limits in patients with unilateral hemispheric stroke and patients with unilateral peripheral 9th and 10th cranial nerve palsies. CONCLUSIONS: Although in WS the lesion due to LMI is unilateral, its effect on oropharyngeal swallowing is bilateral. In LMI, primarily the premotor neurons in the nucleus ambiguous and their connections seem to be affected. Consequently, a disruption and/or disconnection of their linkage to swallowing-related cranial motor neuron pools bilaterally and to the contralateral nucleus ambiguous could produce the swallowing disorders in WS. However, the remaining intact ipsilateral premotor neurons and the contralateral center in the medulla oblongata may eventually begin to operate and overcome the severity and long-term persistence of dysphagia. (+info)
Neurofibromatosis type 1 with basilar artery fusiform aneurysm manifesting Wallenberg's syndrome.
(7/40)
A case of neurofibromatosis type 1 (NF1) manifesting Wallenberg's syndrome and fusiform aneurysm of the basilar artery is reported. The patient suddenly developed dysarthria, walking difficulty and sensory disturbance. Neurological examination suggested Wallenberg's syndrome and MR imaging confirmed an ischemic lesion at the left lateral medulla oblongata. Cerebral angiography revealed a fusiform aneurysm at the middle portion of the basilar artery. However, there was no occlusive change in either the posterior inferior cerebellar artery or the vertebral artery. The clinical and radiological features are discussed together with a review of NF1 cases with intracranial aneurysms in the literature. (+info)
Delayed central respiratory dysfunction after Wallenberg's syndrome--case report.
(8/40)
A 68-year-old man presented with Wallenberg's syndrome consisting of ataxia, dysphagia, hypesthesia on the left side of the body, and Horner's syndrome on the right. Magnetic resonance (MR) imaging revealed a right lateral medullary infarction and small multiple lacunae scattered in the upper medulla. Neurological symptoms improved in a week and the patient was discharged with mild residual hypesthesia on the left side. However, 31 days later, he was emergently admitted after suddenly becoming apneic and losing consciousness. MR imaging detected no new lesion. The patient was placed under ventilation support for 48 hours before regaining normal respiratory function. Medullary infarction sometimes causes catastrophic respiratory failure, but Wallenberg's syndrome caused by lateral medullary infarction is rarely associated with central respiratory dysfunction, and delayed onset of central respiratory dysfunction is extremely unusual. Delayed onset of central respiratory failure is a life-threatening complication of the medullary infarction causing Wallenberg's syndrome, which in general is not recognized. (+info)