Lacunar syndrome due to neurocysticercosis

Seven patients with neurocysticercosis presented with a lacunar syndrome. Four patients had sensorimotor stroke, two had pure motor hemiparesis, and one had ataxic hemiparesis. In every patient, computed tomography or magnetic resonance imaging or both showed a lacunar infarct that was secondary to the occlusion of a terminal vessel affected by endarteritis and was most commonly associated with cysticerci in the suprasellar cistern. Diagnosis of neurocysticercosis was difficult on clinical grounds, but proper integration of data from computed tomography and cerebrospinal fluid analysis provided an accurate diagnosis in every case. Neurocysticercosis should be considered in the differential diagnosis of young adults with a lacunar syndrome who come from areas of the world where this disease is endemic.     

Vertebrobasilar insufficiency due to Tumoural emboli.

A case, which is clinically characterized by a subacute vertebrobasilar syndrome, is presented. The necropsy reveals multiple infarcts in brainstem, cerebellum and left cerebral hemisphere, due to tumoural emboli of a non-detected primary tumour. It is postulated that the latter has to originate in the lungs in order to produce this unique type of cerebral arterial embolism.     

Lacunar syndromes due to brainstem infarct and haemorrhage.

Nine patients with brainstem infarct and two with brainstem haemorrhage presented with pure motor stroke, pure supranuclear facial palsy, sensorimotor stroke or ataxic hemiparesis. Despite the clinical similarity with hemispheric lacunes, brainstem infarcts causing lacunar syndromes probably have a greater tendency to progress. Small brainstem haemorrhages should also be considered as a cause of lacunar syndromes and the difficulty in differentiating them from small infarcts without CT is emphasised.     

Lacunar syndrome due to intracerebral hemorrhage

It has been recognized that small intracerebral hemorrhage not uncommonly produced lacunar syndromes. In this study, we examined cases of intracerebral hemorrhage presenting as lacunar syndromes. Of 174 cases with recent intracerebral hemorrhage, 19 presented with a lacunar syndrome: 4 presented with pure motor hemiparesis, 5, ataxic hemiparesis, 3, dysarthria-clumsy hand syndrome, 7, sensorimotor stroke, and, none, pure sensory stroke. The sites of hemorrhage were capsular in 11, putamenal in 6, and pontine in 2. In these 19 patients, 17 were hypertensive, and the signs characteristic of parenchymal hemorrhage, e.g., gradual onset, headache, nausea, vomiting and stiff neck, were absent or very rare. Computed tomography revealed that one third of the patients had one or more non-symptomatic lacunae in the basal ganglia, the corona radiata or the anterior limb of the internal capsule. These observations suggests that hypertensive intracerebral hemorrhage causes lacunar syndrome more often than previously considered and is apt to manifest ataxic hemiparesis and sensorimotor stroke. Computed tomography is the only way of differentiating hemorrhagic "lacunar" syndrome from lacunar infarct.     

Lacunar syndromes due to intracerebral hemorrhage]

Nine cases (seven men and two women, mean age 64.5 years) of classical lacunar syndromes due to intracerebral hemorrhage are reported. Three patients presented with pure motor hemiparesis (two putaminal hematomas with proportional weakness and one cortical hemorrhage with brachio-crural hemiparesis). Four patients presented with sensorimotor stroke due to thalamo-capsular hemorrhage. The last two patients had thalamic hemorrhage causing ataxic hemiparesis or dysarthria-clumsy hand syndrome. Four subjects had arterial hypertension, one was diabetic, and two were treated with anti-vitamin K. Abrupt onset was noted in all instances. Only one patient experienced moderate inaugural headaches. Good recovery occurred in all cases. Lacunar syndromes are a very uncommon presentation of intracerebral bleeding. Hemorrhages are yet the second etiology of such syndromes. Distinguishing hemorrhage from infarction is not clinically possible and needs early unenhanced CT scan.     

Concomitants of asymptomatic retinal cholesterol emboli.

BACKGROUND AND PURPOSE: Asymptomatic retinal cholesterol emboli are sometimes encountered on ophthalmoscopic examination. They are associated with decreased survival, but their clinical significance is not fully known. We sought to determine which vascular risk factors are associated with such emboli. METHODS: We studied 70 consecutive men (55-84 years old) with asymptomatic retinal cholesterol emboli diagnosed in an eye clinic. Twenty-one men (57-78 years old) from the same eye clinic without retinal emboli or retinal ischemic events were randomly selected as control subjects. We determined vascular risk factors, presence of ischemic heart disease, and extracranial carotid artery disease. RESULTS: Patients had a higher prevalence of hypertension, smoked more, and had a higher prevalence of heterogeneous or echolucent carotid plaques on either side than did control subjects (p less than 0.001 for all three factors). Patients also had a higher prevalence of carotid artery stenosis greater than or equal to 50% on either side and a higher prevalence of ischemic heart disease than did control subjects, but these did not reach statistical significance (p = 0.06 and p = 0.08, respectively). CONCLUSIONS: Our findings suggest that hypertension and cigarette smoking may be important in the pathogenesis of asymptomatic retinal cholesterol emboli and that these emboli indicate systemic atherosclerosis rather than ipsilateral carotid artery stenosis.     

Clinical characteristics of pathologically proved cholesterol emboli to the brain

Cholesterol emboli (CE) to the brain are an important but often unrecognized cause of stroke. The authors reviewed 29 cases of brain CE identified on autopsy. Most patients were elderly (mean age, 74 years) and presented with encephalopathy and acute renal failure. Ten patients developed symptoms spontaneously, 19 after a procedure involving manipulation of the aorta. Brain imaging revealed multiple, small ischemic lesions and border zone infarcts in 11 of 17 patients. Pathology in most patients demonstrated multiple CE mixed with emboli of other types.     

Case report: organic brain syndrome due to multiple tumour emboli

Summary A case of rapid neurological deterioration in a 60-year-old man with oesophageal carcinoma is reported. He sufferred two episodes of global cerebral dysfunction following traumatic endoscopic manipulation. Autopsy findings showed multiple tumour emboli which occluded medium and small-sized vessels in cortical and subcortical areas, resulting in multiple microinfarcts.     

Basilar artery occlusion due to mucormycotic emboli, preceded by acute hydrocephalus

A rare case of brain stem infarction caused by mucormycotic emboli, preceded by acute hydrocephalus, is reported. The patient, who had suffered from leukemia and had undergone bone marrow transplantation several months before, presented initially with seizure and persistent disturbance of consciousness. A head CT scan revealed marked ventricular dilation and diagnosed as acute hydrocephalus. The patient received emergent ventricular drainage. Despite the aggressive treatment, the patient did not survive. Autopsy revealed systemic mucormycosis occluding and invading various arteries including basilar artery and its branches, causing fatal brainstem infarction. Although early diagnosis remains difficult in the cases of systemic mucormycosis, prompt initiation of treatment is mandatory; one must have in mind the possibility of presence of fungal infection when treating patients with acute neurological deterioration who have underlying debilitating diseases, even though fungi themselves are hard to detect in most cases.     

Pure monoparesis of the leg due to cerebral infarctions: A diffusion-weighted imaging study

Pure monoparesis of the leg due to cerebral infarction is rare compared to that of the hand. The anterior cerebral artery (ACA) territory is the most common lesion site in leg monoparesis, but diffusion-weighted (DW) MRI has not commonly been used for lesion detection. The purpose of this study was to use DW MRI to evaluate the radiological correlation with lesion location in patients presenting with pure leg monoparesis. We retrospectively studied six cerebral infarct patients with pure leg monoparesis who had undergone DW MRI. Patients were scanned within 3 days of symptom onset. DW MRI identified lesions in the posterior limb of the internal capsule (PLIC) in two patients, in the corona radiata (two patients), in the subcortical white matter of the posterior frontal lobe (one patient), and in the frontal and parietal cortex, including the paracentral lobule and precuneus (one patient). The two patients with PLIC infarctions had characteristic linear infarction abnormalities along the long axis of the internal capsule. Corona radiata infarction were located posteriorly, and the two subcortical and cortical infarction were thought to be in the territory of the ACA. We thus concluded that in leg monoparesis due to infarctions, lesions may be located in the PLIC, corona radiata, or in the ACA territory. Recently, magnetic resonance tractography has shown that foot fibres of the corticospinal tract in the PLIC somatotopically may be posteromedial to hand fibres along the short axis of the internal capsule, rather than posterolateral along the long axis as has been thought. Thus, damage along the long axis of the PLIC by linear infarctions can cause pure monoparesis of the leg.     

Cholesterol masses in association with spinal cord infarction due to intervertebral disc emboli

Summary The clinical and autopsy findings are presented from three dogs with spinal cord infarction. At autopsy firm gritty masses and cystic areas were present within the spinal cord. The masses contained numerous cholesterol clefts, collagen and reticulin fibres and were accompanied by a macrophage, giant cell and lymphocytic reponse. The cholesterol masses were present mainly in white matter. The ventral spinal artery or its branches as well as pial arteries contained fibrillary masses often covered by endothelial cells. The staining characteristics of these emboli suggested that they were fibro-cartilagenous and probably derived from the intervertebral discs. It is assumed that the cholesterol masses were formed from myelin breakdown products within infarcted areas.     

Lacunar stroke. A reassessment

Lacunae are small, deep cerebral infarcts known to occur in hypertensive patients. Although frequently asymptomatic, they sometimes produce characteristic clinical syndromes. Postmortem studies have implicated small-vessel disease in their pathogenesis, and, as a result, conservative management has been advocated. Computed tomography (CT) has provided new insights into the spectrum of lacunar disease. Review of recently acquired information suggests modifications of the approach to these patients. The clinical lacunar syndromes, though nonspecific, do suggest lacunar infarction. In hypertensive patients with these syndromes and CT confirmation of lacunar infarction, a conservative diagnostic posture coupled with medical management of risk factors continues to be indicated.     

Treatment Approaches to Lacunar Stroke

Lacunar strokes are appropriately named for their ability to cavitate and form ponds or “little lakes” (Latin: lacune -ae meaning pond or pit is a diminutive form of lacus meaning lake). They account for a substantial proportion of both symptomatic and asymptomatic ischemic strokes. In recent years, there have been several advances in the management of large vessel occlusions. New therapies such as non-vitamin K antagonist oral anticoagulants and left atrial appendage closure have recently been developed to improve stroke prevention in atrial fibrillation; however, the treatment of small vessel disease-related strokes lags frustratingly behind. Since Fisher characterized the lacunar syndromes and associated infarcts in the late 1960s, there have been no therapies specifically targeting lacunar stroke. Unfortunately, many therapeutic agents used for the treatment of ischemic stroke in general offer only a modest benefit in reducing recurrent stroke while adding to the risk of intracerebral hemorrhage and systemic bleeding. Escalation of antithrombotic treatments beyond standard single antiplatelet agents has not been effective in long-term lacunar stroke prevention efforts, unequivocally increasing intracerebral hemorrhage risk without providing a significant benefit. In this review, we critically review the available treatments for lacunar stroke based on evidence from clinical trials. For several of the major drugs, we summarize the adverse effects in the context of this unique patient population. We also discuss the role of neuroprotective therapies and neural repair strategies as they may relate to recovery from lacunar stroke.     

Atheromatous emboli to the lumbosacral spinal cord.

The lumbosacral spinal cords of 28 patients with atheromatous emboli to abdominal viscera and/or grafts to the abdominal aorta were examined by serial sections. In 12 patients, atheromatous emboli were found in spinal arteries, most commonly in the sacral cord, and most frequently in the anterior spinal artery. The general absence of spinal cord infarctions was attributed to the nature of the emboli, apparent good collateral circulation, and the absence of diffuse atherosclerosis. However, 38% of the patients had arteriosclerosis; this was generally focal and not associated with significant luminal narrowing. Only one patient had infarction, which was limited primarily to the gray matter. It would appear that hypoperfusion must exist in conjunction with atheromatous emboli in order for infarction to develop. Organized atheromatous emboli also caused focal ischemic atrophy of neurons. It is postulated that this change may be the morphological basis for some of the atypical lower motor neuron diseases found in the elderly.     

Locked-in syndrome due to bilateral cerebral peduncular infarctions with occlusion of persistent primitive trigeminal artery]

A 61-year-old woman with diabetes mellitus was admitted to our hospital with right hemiparesis and dysarthria. Brain MRI showed bilateral cerebral peduncular infarctions. Three days after admission, she was unable to generate any voluntary movements, except for those of the eye, suggesting locked-in syndrome (LIS). She could not speak, but showed good comprehension by blinking in response to verbal commands. Brain CT 5 days later revealed subarachnoid hemorrhage (SAH) around quadrigeminal and ambient cistern. Cerebral angiogram on the following day revealed no aneurysm, occlusion of right persistent primitive trigeminal artery (PPTA) and a little flow of the bilateral vertebral arteries. Eye movements were impossible in all directions on the 11th day and MRI showed new infarctions of the midbrain and the ventral portion of the pons. However, an EEG on the 20th day was almost normal. We speculated that low blood flow in the basilar artery from the PPTA caused bilateral cerebral peduncular infarctions, and that weakness of the PPTA caused SAH.     

Cholesterol emboli neuropathy.

We report the clinical and pathologic features of a patient with peripheral neuropathy that was the first clinical expression of cholesterol emboli syndrome (CES). Biopsy of skeletal muscle and peripheral nerve revealed cholesterol clefts in lumens of small arteries, necrotizing arteritis, and severe degeneration of peripheral and intramuscular nerves. At autopsy, the peripheral nervous system was extensively affected by similar changes. We conclude that (1) peripheral neuropathy may be the initial manifestation of CES. Presumably, deposition of cholesterol leads to arteritis. (2) The underlying pathology of CES neuropathy is chronic axonal degeneration, possibly due to chronic ischemia of epineurial arteries. (3) Muscle biopsy is important in the antemortem diagnosis of CES. Nerve biopsy may show involvement of epineurial vessels. (4) CES may resemble polyarteritis nodosa clinically and pathologically. (5) CES may be under-recognized and should be included in the differential diagnosis of any neuropathy of uncertain cause, particularly when there is a history of vascular catheterization, or severe aortic atherosclerosis.