Diffusion-weighted imaging identifies a subset of lacunar infarction associated with embolic source. (1/65)

BACKGROUND AND PURPOSE: Small infarcts in the territory of penetrator arteries were described as causing a number of distinct clinical syndromes. The vascular pathophysiology underlying such infarcts is difficult to ascertain without careful pathological study. However, the occurrence of multiple, small infarcts, linked closely in time but dispersed widely in the brain, raises the possibility of an embolic mechanism. The current study determines the frequency and clinical characteristics of patients with well-defined lacunar syndromes and the diffusion-weighted imaging (DWI) evidence of multiple acute lesions. METHODS: Sixty-two consecutive patients who presented to the emergency room with a clinically well-defined lacunar syndrome were studied by DWI within the first 3 days of admission. RESULTS: DWI showed multiple regions of increased signal intensity in 10 patients (16%). A hemispheric or brain stem lesion in a penetrator territory that accounted for the clinical syndrome ("index lesion") was found in all. DWI-hyperintense lesions other than the index lesion ("subsidiary infarctions") were punctate and lay within leptomeningeal artery territories in the majority. As opposed to patients with a single lacunar infarction, patients with a subsidiary infarction more frequently (P<0.05) harbored an identifiable cause of stroke. CONCLUSIONS: Almost 1 of every 6 patients presenting with a classic lacunar syndrome has multiple infarctions demonstrated on DWI. This DWI finding usually indicates an identifiable cause of stroke and therefore may influence clinical decisions regarding the extent of etiologic investigations and treatment for secondary prevention.  (+info)

Sensory sequelae of medullary infarction: differences between lateral and medial medullary syndrome. (2/65)

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)

Xenon contrast-enhanced CT imaging of supratentorial hypoperfusion in patients with brain stem infarction. (3/65)

BACKGROUND AND PURPOSE: The characteristics of hypoperfusion in the supratentorial region of patients with brain stem infarction are unclear. We investigated the relationships between the presence of hypoperfusion and the location, number, and size of the infarcts with xenon contrast-enhanced CT. METHODS: One hundred five patients with brain stem infarction detected by MR imaging underwent xenon contrast-enhanced CT to measure the regional CBF (rCBF) in the frontal, temporal, parietal, and occipital regions and in the putamen and thalamus. A decrease of more than 10% from the mean rCBF value for normal individuals was considered to indicate hypoperfusion. RESULTS: Thirty-six patients had supratentorial hypoperfusion. The mean rCBF values (measured in mL/100 g/minute) were as follows: frontal region, 36.2 +/- 5.1 (-14.8%, n = 28); parietal region, 42.3 +/- 4.7 (-19.1%, n = 29); temporal region, 41.5 +/- 2.8 (-12.6%, n = 12); and thalamus, 50.1 +/- 3.2 (-19.6%, n = 7). Supratentorial hypoperfusion was associated with pontine infarction in 33 patients (upper pons in 15, middle pons in 18, and lower pons in seven), midbrain infarction in two, and medulla infarction in one. Twenty-three patients had infarcts that were larger than 5 mm, and 11 had infarcts that were 2 to 5 mm. Only two had infarcts that were smaller than 2 mm. Seven patients each had one infarct, 13 each had two, and 16 each had three. CONCLUSION: Supratentorial hypoperfusion was associated with larger infarcts, with more infarcts, and with pontine infarction.  (+info)

Course and distribution of facial corticobulbar tract fibres in the lower brain stem. (4/65)

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.  (+info)

Neuroimaging in deteriorating patients with cerebellar infarcts and mass effect. (5/65)

BACKGROUND AND PURPOSE: The decision to proceed with surgery in cerebellar infarct with mass effect (CIMASS) in deteriorating patients is based on clinical features. The potential role of neuroimaging in predicting deterioration has not been systematically studied. In this study we determine the role of neuroimaging in predicting deterioration in CIMASS. METHODS: -We retrospectively reviewed the clinical and neuroimaging features in 90 patients with cerebellar infarcts. We selected for detailed analysis CIMASS in 35 patients. RESULTS: Eighteen patients remained stable and 17 deteriorated. Of these 17 patients, 8 were treated conservatively and 9 had surgery. Radiological features indicative of progression were more common in deteriorating patients compared with stable patients: fourth ventricular shift (82.3% versus 50%, P:=0.075, OR=4. 67), hydrocephalus (76.5% versus 11.1%, P:=0.0001, OR=26), brain stem deformity (47% versus 5.6%, P:=0.0065, OR=15.1), and basal cistern compression (35.3% versus 0%, P:=0.0076, OR=20.91). Differences in upward displacement of the aqueduct and pontomesencephalic junction from Twining's line, tonsillar descent on sagittal MRI, and infarct volumes between stable and deteriorating patients were not statistically significant. CONCLUSIONS: Hydrocephalus, brain stem deformity, and basal cistern compression may herald deterioration in CIMASS. Admission to a neurological-neurosurgical intensive care unit and consideration of preemptive surgery are warranted in these patients. Vertical displacement of tonsils or aqueduct, demonstrated by MR imaging, did not predict deterioration.  (+info)

Dissecting aneurysm of the vertebral artery causing subarachnoid hemorrhage after non-hemorrhagic infarction--case report. (6/65)

A 45-year-old male presented with lateral medullary infarction. Cerebral angiography showed dissecting aneurysm as pearl and string sign in the right vertebral artery (VA). Conservative treatment was administered with antiplatelet agent. However, subarachnoid hemorrhage occurred 2 days after admission, inducing coma. Intraaneurysmal embolization and proximal occlusion of the right VA by intravascular surgery resulted in only mild neurological deficits. Conservative treatment including strict control of blood pressure is the first choice of treatment. Antiplatelet therapy and anticoagulant therapy should not be administered. Patients must be followed up by serial angiography and surgery considered if signs of aneurysmal progression are seen.  (+info)

Neurological complications of cervical spine manipulation. (7/65)

To obtain preliminary data on neurological complications of spinal manipulation in the UK all members of the Association of British Neurologists were asked to report cases referred to them of neurological complications occurring within 24 hours of cervical spine manipulation over a 12-month period. The response rate was 74%. 24 respondents reported at least one case each, contributing to a total of about 35 cases. These included 7 cases of stroke in brainstem territory (4 with confirmation of vertebral artery dissection), 2 cases of stroke in carotid territory and 1 case of acute subdural haematoma. There were 3 cases of myelopathy and 3 of cervical radiculopathy. Concern about neurological complications following cervical spine manipulation appears to be justified. A large long-term prospective study is required to determine the scale of the hazard.  (+info)

Massive pontine hemorrhagic infarction associated with embolic basilar artery occlusion. (8/65)

We report here an autopsy case of massive pontine hemorrhagic infarction secondary to embolic basilar artery occlusion. A large embolus appeared to have traversed the vertebral artery into the basilar artery as a result of basilarization of the vertebral artery due to severe stenosis of the contralateral vertebral artery. Extensive ischemia due to embolic occlusion of the entire length of the basilar artery, and migration of the embolus are assumed to have resulted in a massive pontine hemorrhagic infarction.  (+info)

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