Adrenalectomy does not affect the nocturnal peak of Fos expression within hypothalamic pro-opiomelanocortin neurons

Clinical and evoked-potential studies in internal capsule and corona radiata infarction are lacking. We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction. Patients's outcome was defined at the end of 3 months on the basis of the Barthel Index score. Four patients with type A capsular infarction (middle third of posterior limb of internal capsule) all had severe weakness, while 2 also had persistently unrecordable CMCT and poor outcome. Twelve patients with type B internal capsular infarction (genu, anterior limb, anterior or posterior third of posterior limb) had a milder degree of weakness, and CMCT was recordable in 9. At 3 months' follow-up, however, CMCT was recordable in all 12 patients. All of these patients had a partial (n = 4) or complete (n = 5) recovery. Thirteen patients with type A corona radiata infarction (middle third of corona radiata) had more pronounced weakness, and CMCT was unrecordable in all of these patients except 1 on initial examination. Follow-up after 3 months was possible in 8 patients, and CMCT became recordable in 3. One of these patients had complete, 3 partial, and 4 poor recovery. In type B corona radiata infarction (anterior or posterior third of corona radiata), the clinical signs and CMCT did not follow a regular pattern. Clinical and CMCT abnormalities in internal capsular infarction followed a more predictable pattern compared with those in corona radiata infarction. A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule.     

Blockade of morphine- and amphetamine-induced conditioned place preference in the rat by riluzole

Three cases of isolated one-and-a-half syndrome with facial nerve palsy related to infarction are presented. Magnetic resonance imaging in cases 1 and 2 was unremarkable, whereas magnetic resonance angiography demonstrated pathophysiologically significant vertebral basilar disease. Case 3 is unique due to its association with giant cell arteritis. Ipsilateral adduction improved to a greater extent than abduction in each case, perhaps providing insight into the exact localization of these lesions or selective vulnerability of the ocular motor structures within the pons. This combination of clinical findings, termed the 8-1/2 syndrome (cranial nerve 7 + 1-1/2), allows precise localization, and magnetic resonance angiography appears to be the imaging study of choice.     

Somatosensory evoked potential studies in internal capsule and corona radiata infarction

To document the somatosensory evoked potential (SEP) changes in capsular and corona radiata infarction and correlate these with clinical and radiological findings, 15 patients with corona radiata and 16 with internal capsular infarction were studied. The mean age of the patients was 55 years (range 26-80), and 6 of them were female. In the patients with corona radiata infarction, median N9-N20 conduction time was abnormal in 4 cases, which correlated with sensory abnormalities in 1. In 3 of these patients, infarction was located in the anterior two-thirds and in 1 there was total corona radiata infarction. The amplitude of N20 potential on the affected side was reduced in 1 patient. In the capsular infarction group, N9-N20 conduction time was abnormal in 1 patient only who had total involvement of the posterior limb of the internal capsule. The amplitude of N20 was reduced in another patient. There were 4 patients who had abnormal sensory findings, but their SEPs were normal. At 3 months, the SEP changes remained stable in all of the patients who were followed up. The SEP changes did not correlate with changes in sensation or 3-month outcome as assessed by the Barthel index score. The lack of clinicoradiological and SEP correlation may be owing to variation on the organisation of sensory pathways in the corona radiata and internal capsule.     

Cerebral infarction associated with nephrotic syndrome in a young adult: a case report

We report a 19-year-old man who developed a cerebral infarction in the territory of the anterior choroidal artery and showed a hypercoagulable state and nephrotic syndrome after diarrhea and appetite loss. He had suffered from nephrotic syndrome from the age of three and had been treated for five years. MR-angiography showed an occlusion originating in the right internal carotid artery. The right anterior and middle cerebral arteries were imaged from the left internal carotid artery via the anterior communication artery. He showed symptoms of left hemiparesis, agnosia, loss of activity, anasarca and left hypacusis following his clinical course, but had recovered from all but left hemiparesis following medical treatments including steroid therapy. The histologic finding by a renal biopsy revealed focal glomerulosclerosis. In this case, we considered that when he was in a hypercoagulable state and had a second attack of nephrotic syndrome because of inflammation and dehydration due to diarrhea and appetite loss, his hypercoagulable state grew worse, and he then developed a cerebral infarction. When one see a patient with nephrotic syndrome, one should be attentive to the possibility of a complication of cerebral infarction.     

Focal corneal decompensation caused by an anterior capsulotomy remnant

Capsule contraction syndrome, an infrequent but sight-compromising condition, can usually be managed by a neodymium:YAG (Nd:YAG) anterior capsulotomy. The anterior capsule can be split from the visual axis to the periphery with multiple spokes. In this patient, however, these spokes closed, leaving the small anterior capsulotomy indistinguishable from its pre-capsulotomy appearance. A subsequent Nd:YAG laser circumcision of the thickened capsulotomy margin restored the patient's sight. The excised capsular doughnut fell into the anterior chamber angle and resulted 34 months later in localized corneal decompensation. Removal of the capsular remnant markedly improved the corneal changes. The experience from this case suggests that multiple Nd:YAG relaxing incisions may be a safer way to manage capsule contraction syndrome than complete circumcision of the anterior capsule. If the latter approach is taken, the capsular remnant should not be cut completely free of the anterior capsule.     

Severe tricuspid insufficiency as main manifestation of hyperthyroidism

Infarction in the territory of the posterior spinal arteries is uncommon, giving rise to a softening of variable extend in the peripheral arterial system. In the reported case, the lesion was restricted to a posterior column and produced a syndrome of crural ataxic hemiparesis.     

In memoriam John R Casely-Smith, D. Sc., M.D. (h.c.)

BACKGROUND: After curvilinear capsulorhexis in cataract surgery often a double-ring shape of the remaining capsular margins can be observed. In order to better understand this phenomenon we performed a histological study of excised capsules after continuous curvilinear capsulorhexis. METHODS: Ten anterior capsular specimens from cases with double-ring structure of the capsular margins after continuous curvilinear capsulorhexis (D-group) were examined light microscopically and compared with 10 normal cases (N-group) and 10 cases with pseudoexfoliation (P-group). Three cases from each group were also examined electron microscopically. RESULTS: A characteristic step formation in the capsular edges and in addition horizontal capsular splits in the border zone between the zonular lamella of the anterior capsule and the capsule proper could be demonstrated histologically in the D-group. CONCLUSIONS: There seems to be a weak point of the capsular tissue in the border zone between zonular lamella of the lens and the capsule proper. The superficial splits that we found histologically in this region might be a precursor or forme fruste of true exfoliation. The outward-directed traction force exerted by the zonular fibers seems to lead to further disruption in this weakened layer of the lens capsule during capsulorhexis, producing a double-ring contour of the capsular margins.     

A case of pontine infarction with persistent primitive proatlantal artery

A 61-year-old woman was admitted to the hospital on September 18, 1991 because of left hemiparesis, dysphagia, and dysarthria since five days before. She was formerly pointed out diabetes mellitus and hypertension, but she did not receive any treatment. The MRI showed a high signal area in the right paramedian portion of the upper pons on T2 weighted image and proton image. The angiography showed that persistent primitive proatlantal artery originated from the left internal carotid artery and joined to the horizontal portion of the left vertebral artery. The image of carotid-vertebrobasilar system and proatlantal artery showed so severely arteriosclerotic. This is the first report of brainstem infarction with persistent primitive proatlantal artery. In this case, the pontine infarction was thought to occur on the basis of the arteriosclerosis of blood vessels and change of blood flow of carotid-vertebrobasilar system due to persistent primitive proatlantal artery.     

Medial medullary infarct

Medial medullary infarct is a rare type of brain stem infarction first described in 1908. It was only since the broad use of MRI that an accurate clinical topographical correlation could be documented in survivors. We observed two patients; one of them had an anteromedial unilateral infarction in the upper medulla, and the clinical picture was characterized by contralateral hemiparesis, facial weakness, dysarthria and palatal weakness. The outcome was good. The second patient however showed a severe tetraparesis with only minor brain stem signs, secondary to bilateral anteromedian infarction with a large craniocaudal extension. He survived with severe residual impairment. The most likely cause of infarction was arteriosclerosis of the A. vertebralis and A. spinalis anterior, respectively. These two different cases suggest that the medial medullary syndrome is heterogeneous comprising small unilateral infarctions with mild clinical signs as well as large bilateral infarctions with a poor outcome.     

Effect of extracranial carotid artery stenosis and other risk factors for stroke on periventricular hyperintensity

BACKGROUND AND PURPOSE: The pathogenesis of periventricular hyperintensity (PVH) is still uncertain. We investigated the relationship between PVH and risk factors for cerebrovascular diseases, especially extracranial carotid artery stenosis (ECAS). METHODS: We studied PVH and ECAS in 323 subjects between 1991 and 1994. Using 1.5-T MRI scan images, we measured PVH quantitatively at eight points and evaluated cerebral infarction. Duplex carotid sonography was performed on the carotid arteries bilaterally and used to divide the severity of ECAS into five grades. Risk factors for cerebrovascular diseases and atherosclerotic complications were assessed from the clinical history. RESULTS: Age was significantly correlated with the size of frontal and whole PVH (P < .01). Frontal PVH was significantly more severe in subjects with hypertension (P < .05). Frontal, occipital, and whole PVH were significantly more severe in subjects with a history of cerebrovascular accident (P < .01). Other risk factors and atherosclerotic complications were not correlated with PVH. There were no significant differences in the severity of PVH among the five groups of ECAS. The severity of PVH in each region was not related to ECAS. There was no significant difference in the age of patients in relation to the five grades of ECAS. However, PVH was significantly more severe in subjects with lacunar infarction or infarction of the deep border zone (P < .05). There was no relationship between PVH and cortical infarction or infarction of the cortical border zone. CONCLUSIONS: PVH correlated with age, hypertension, and past history of cerebrovascular disease but not with ECAS. PVH was significantly more severe in lacunar infarction and infarction of the deep border zone. These results suggest that small-vessel disease may underlie the pathogenesis and development of PVH.     

Moyamoya and Down syndrome. Clinical and radiological features

BACKGROUND AND PURPOSE: Moyamoya disease is a chronic occlusive cerebrovascular disorder characterized by progressive stenosis of the supraclinoid internal carotid artery, with the secondary development of enlarged basal collateral vessels. It may occur as a primary disease or as a syndrome in association with a variety of conditions, and its pathogenesis remains unexplained. There are relatively few reports describing the occurrence of moyamoya in Down syndrome. The aim of this study is to describe the clinical and radiological features of moyamoya syndrome associated with Down syndrome (MM-DS) and to explore theories of moyamoya pathogenesis in these patients. METHODS: Seven children with MM-DS underwent brain imaging, transfemoral angiography, and serial neurological exams. Neurological deficits, poststroke recovery, radiographic infarct characteristics, and angiographic abnormalities were reviewed. RESULTS: The clinical and radiological features of primary moyamoya disease overlap with those of MM-DS. Hemiplegia and aphasia were the most common presentations. Motor recovery was excellent in five of seven cases. Cerebral infarcts were superficial or deep and can occur in a watershed distribution. Angiography demonstrated involvement of the internal carotid artery and its branches bilaterally in all seven cases and the posterior cerebral arteries in four cases. CONCLUSIONS: The clinical and radiological features of MM-DS overlap with primary moyamoya disease. We postulate that a protein encoded on chromosome 21 may be related to the pathogenesis of moyamoya disease. Although the neuronal substrate is abnormal in Down syndrome patients, recovery from hemiplegic stroke in patients with MM-DS is comparable to recovery in patients with primary moyamoya.     

Calcification of lumbar ligamentum flavum and facet joints capsule

STUDY DESIGN: The incidence of calcification in ligamentum flavum and posterior capsule demonstrated by computed tomography was reviewed in a series of 147 patients in whom 419 lumbar levels were studied. OBJECTIVES: To find a relationship between mechanical lumbar pathology and the calcification of the ligamentum flavum and posterior capsule. SUMMARY OF BACKGROUND DATA: Calcification of the ligamentum flavum and posterior capsule has been found in diffuse idiopathic skeletal hyperostosis and in metabolic disorders. Although this fact is considered a manifestation of degenerative disease of the spine, it barely has been studied, and many questions remain unresolved. METHODS: Calcifications were classified according to location as follows: 1) ligamentum flavum: upper attachment, lateral or capsular extension, caudal attachment, interlaminar portion or 2) posterior capsule. RESULTS: The following statistical associations were found: 1) degenerative facet joint disease with posterior capsule and lateral or capsular extension calcifications, 2) lumbarized vertebra with lateral or capsular extension and upper attachment calcifications, and 3) isthmic spondylolisthesis with lateral or capsular extension calcification.     

Severe complications after breast reduction]

The neuropathology of narcolepsy is unknown. Recently, Plazzi et al. (1) reported magnetic resonance imaging (MRI) abnormalities in the pontine tegmentum of three patients with long-standing idiopathic narcolepsy. Considering the localization of the neuroradiological findings in the pontine reticular formation, where rapid eye movement (REM) sleep is generated, the authors suggested a causal relationship between narcolepsy and MRI abnormalities. Frey and Heiserman, however, found pontine MRI abnormalities in only two of 12 patients with narcolepsy both of whom had long-standing hypertension (2). Pullicino et al. noted similar pontine MRI abnormalities in patients with subcortical arteriosclerotic encephalopathy-like ischemic rarefaction of the pons (3). Thus, the changes noted by Plazzi et al. may have been caused by small-vessel disease rather than narcolepsy. To assess whether altered pontine MRI signals are a regular feature of idiopathic narcolepsy, we selected randomly from our database seven patients with narcolepsy with cataplexy. Of these seven, three agreed to have brain MRIs; their cases are described below. None had pontine MRI abnormalities.     

Sonographically guided placement of peripherally inserted central venous catheters: review of 355 procedures

OBJECTIVE: To test whether Wallerian degeneration (WD) of the pyramidal tract as signaled by MRI affects rehabilitation outcome in patients with subcortical infarction (internal capsule or corona radiata). BACKGROUND: Recent radiologic evidence suggests that WD occurs no earlier than 3 months after a subcortical infarction. METHODS: A total of 77 consecutive patients with pure motor hemiparesis due to an initial subcortical infarction were assessed on admission and discharge with the Functional Independence Measure (FIM) for disability and Stroke Impairment Assessment Set (SIAS, full = 25) for impairment. WD was defined by a high-intensity area detected along the pyramidal tract below the level of lesion on T2-weighted MR image (WD+). RESULTS: Age, sex, side of stroke, Mini-Mental State Examination score, and volume of lesion were comparable for each group. Length of stay (LOS) was significantly longer (p < 0.05) in WD+ (130 days) than in WD- (105 days). There was no difference in the change of FIM (WD+, 99 to 111; WD-, 95 to 107) or SIAS measures (WD+, 12 to 16; WD-, 13 to 16) made on admission and discharge, nor was there any effect of the timing of the rehabilitation experience (< or = 90 days or >90 days after stroke). CONCLUSIONS: After stroke, apparent WD of the pyramidal tract may slow functional recovery but does not limit final rehabilitation outcome of pure motor hemiparesis. Study of the mechanisms of compensation for this delayed pyramidal tract degeneration will enhance the scientific basis for rehabilitation.     

Bithalamic hyperintensity on T2-weighted MR: vascular causes and evaluation with MR angiography

PURPOSE: To determine whether MR angiography can be used to differentiate between the two vascular causes of bithalamic hyperintensity on T2-weighted MR images: "top of the basilar" artery occlusion and deep cerebral vein thrombosis. METHODS: A retrospective review identified six patients with bithalamic T2 hyperintensity of vascular causes. MR angiography was performed in four patients, MR angiography and conventional angiography in one patient, and conventional angiography in one patient. Data pertaining to clinical presentation and hospital course were collected. MR angiographic techniques were multislab overlapping three-dimensional time-of-flight, 2-D time-of-flight, and 2-D phase-contrast. RESULTS: Three cases of top of the basilar artery occlusion and three cases of deep cerebral vein thrombosis were recognized. In all cases, T2 hyperintensity in a vascular distribution suggested cerebral occlusive disease. Infarction involving the thalami and basal ganglia was present in two cases of deep cerebral vein thrombosis. Infarction of the thalami, mesodiencephalic region, and cerebellar hemispheres was present in two cases of basilar artery occlusion. Bithalamic infarction alone was seen in one case of deep cerebral vein thrombosis and one case of basilar artery occlusion. In the five cases in which MR angiography was used, this technique accurately distinguished the vessels involved (arterial or venous). CONCLUSION: MR angiography is a useful adjunct to MR imaging in the evaluation of bithalamic T2 hyperintensity. It does help distinguish between the two vascular causes: top of basilar artery occlusion and deep cerebral vein thrombosis.     

Ophthalmoplegia, hemiparesis and cheiro-oral syndrome in basilar artery migraine

A patient with migraine developed ophthalmoplegia, hemiparesis and cheiro-oral syndrome on the left side. T2-weighted MRI showed infarcts in the tegmentum of bilateral midbrains and right pons but no lesion in the cerebral or cerebellar hemisphere. Infarction in the tegmentum of brainstem secondary to the involvement of perforating arteries has not been reported in basilar artery migraine until now.     

Subarachnoid neurocysticercosis with occlusion of the major intracranial arteries: case report

Cysticercosis is the most common parasitic disease affecting the central nervous system. Stroke is a recognized complication of neurocysticercosis, occurring in 2 to 12% of cases, mostly in the form of small lacunar infarcts. We report a case of hemiparesis and aphasia in a 51-year-old Hispanic woman, which was secondary to complete occlusion of the left internal carotid and bilateral anterior cerebral arteries. Magnetic resonance imaging demonstrated the presence of enhancing subarachnoid material surrounding these occluded cerebral arteries, providing antemortem, noninvasive documentation of the inflammatory meningeal cysticercotic reaction that was presumably responsible for the occlusive arteritis causing the cerebral infarction. This represents the third reported case of internal carotid artery occlusion and the first reported case of anterior cerebral artery occlusion secondary to neurocysticercosis.     

Cervical lymph node metastatic patterns of squamous carcinomas in the upper aerodigestive tract

We report a patient with medial medullary infarction who showed deep sensory impairment as his prominent neurological manifestation. A 54-year-old man with a history of hypertension was admitted to our hospital with numbness of the bilateral upper and lower extremities, followed by dysarthria and right hemiparesis. Physical examination revealed no abnormalities except for high blood pressure. He hiccuped continuously. On neurological examination, he exhibited dysarthria, mild dysphagia and right hemiparesis without facial or lingual paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and thromboxane synthetase inhibitor. His hiccups stopped within two weeks, and his right hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive lupus anticoagulant. MRI showed bilateral infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities. Neurological manifestations of our patient are not typical of medial medullary infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable hiccups to the bilateral medial medullary lesions, and emphasize the importance of lupus anticoagulant as one of the risk factors in brainstem infarction.     

Capsular tension ring in a patient with Weill-Marchesani syndrome

Weill-Marchesani patients with cataractous lenses may presnet a surgical challenge in the presence of zonular weakness and microsherophakia. A 52-year-old Weill-Marchesani patient developed zonular dehiscence during capsule contraction after cataract extraction in her right eye. Use of a poly(methyl methacrylate) capsular tension ring in the second eye facilitated lens removal and intraocular lens placement. Postoperative results suggest the capsular tension ring provides long-term zonular stabilization by maintaining an internal force against the capsule.     

Evaluation of the first 100 consecutive PhacoFlex silicone lenses implanted in the bag through a self-sealing tunnel incision using the Prodigy inserter

We evaluated the performance of the PhacoFlex silicone lens with open polypropylene loops and the disposable Prodigy inserter in a series of 100 consecutive no-stitch cases. Loading the lens into the PRO-1A inserter model was easy, as was inserting it through a 4 x 4 mm self-sealing sclerocorneal tunnel incision. If the chamber was deep and the capsular fornix expanded, unfolding the polypropylene loops was safe and direct bag placement was always possible. If the capsular bag was insufficiently distended, however, the posterior loop tended to entangle with wrinkles in the posterior capsule, jeopardizing the capsule's integrity. With a round and well-centered 4 mm to 5 mm capsulorhexis, centration was good provided the lens was completely within the bag. Even with proper bag placement of the haptics, however, the optic occasionally decentered slightly and tilted because of secondary capture in the capsulorhexis opening. With an incomplete capsulorhexis or a jagged-edged capsulotomy, malpositioning was not uncommon. This was due to secondary displacement of one haptic into the sulcus or partial capture of the optic by the anterior capsule leaf. Because of the flexibility of the polypropylene loops, the lenses tended to decenter and tilt following capsular shrinkage.