Impaired modulation of quadriceps tendon jerk reflex during spastic gait: differences between spinal and cerebral lesions.
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In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents. The changes in modulation of quadriceps tendon jerk reflexes during gait of healthy subjects were compared with those of hemi- or paraparetic spastic patients. The spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during gait was almost removed and was associated with weak or no modulation during the step cycle. In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the 'unaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during gait in healthy subjects are impaired to different extents in spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesis. (+info)
Hemiosteoporosis after severe stroke, independent of changes in body composition and weight.
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BACKGROUND AND PURPOSE: Fractures are a serious complication after stroke, and the risk of hip fractures among stroke patients is increased 2 to 4 times versus a reference population. Fractures after stroke are probably caused by the development of hemiosteoporosis and the high incidence of accidental falls. The aim of this study was to investigate the development of hemiosteoporosis in relation to other changes in body composition during the first year after severe stroke. METHODS: The study included 24 patients with extensive paresis after stroke. Bone mineral content (BMC) and fat and lean mass were assessed 1, 4, 7, and 12 months after stroke onset by a dual-energy x-ray absorptiometer. RESULTS: The loss of total body BMC was significant during the first year after stroke (-1.6%; P<0.05), but there were no significant changes in total lean or fat mass. At inclusion, there were no significant differences between sides in lean or fat mass or BMC, but during follow-up, BMC of the affected side decreased significantly compared with the same side at inclusion (-7.5%; P<0.01). Side differences in fat mass became significant between legs (9.3%; P<0.001) and whole sides (4. 8%; P<0.01). There were only minor side changes in lean mass. Loss of BMC was independent of weight changes. CONCLUSIONS: During the first year after severe stroke, patients developed pronounced hemiosteoporosis. This was not associated with general changes in lean or fat mass. The development of hemiosteoporosis was independent of weight changes after stroke. (+info)
Stereotactic radiosurgery for cavernous sinus cavernous hemangioma--case report.
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A 40-year-old female presented with cavernous sinus cavernous hemangioma manifesting as left abducens and trigeminal nerve pareses. Magnetic resonance imaging revealed a left cavernous sinus tumor. The tumor was partially removed. Histological examination of the specimen confirmed cavernous hemangioma. Radiosurgery was performed using the gamma knife. The tumor markedly decreased in size after radiosurgery and morbidity was avoided. Cavernous sinus cavernous hemangiomas may be difficult to treat surgically due to intraoperative bleeding and cranial nerve injury. Stereotactic radiosurgery can be used either as an adjunct treatment to craniotomy, or as the primary treatment for small cavernous sinus cavernous hemangioma. (+info)
Spinal cord ischemia after abdominal aortic operation: is it preventable?
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PURPOSE: Spinal cord ischemia after operation on the abdominal aorta is a rare event that is attributed to variations in the spinal cord blood supply. The purpose of this study was to evaluate the possible causes of this devastating event. METHODS: A survey of patients among the members of the Southern Association for Vascular Surgery was performed, and 18 patients were identified with spinal cord ischemia manifested by paraplegia or paraparesis after abdominal aortic operation. RESULTS: Preoperative computed tomographic, magnetic resonance, and aortographic results did not visualize the greater radicular artery (Adamkiewicz's artery) in any patient. Eleven patients underwent resection of infrarenal abdominal aortic aneurysms (AAAs): seven of these patients had tube grafts, three had aortobifemoral grafts, and one had an aortobiiliac graft. Five other patients underwent placement of aortobifemoral grafts, and one patient underwent aortobiiliac graft placement for occlusive disease. One patient underwent suprarenal AAA resection with an interposition graft to a previous aortobiiliac graft. The mean operative time was 3 hours and 39 minutes (range, 2 hours and 45 minutes to 6 hours and 30 minutes), with a mean aortic cross-clamp time of 48 minutes (range, 24 to 97 minutes). Sixteen aortic cross-clamps were placed infrarenally and two suprarenally (one in a case of ruptured AAA, the other a suprarenal AAA). Seventeen proximal anastomoses were end to end. The average minimum systolic blood pressure during the aortic cross-clamping was 96 mm Hg (range, 80 to 130 mm Hg). All the patients had internal iliac artery flow preserved with either prograde perfusion (10 patients) or retrograde perfusion (eight patients), and one patient underwent unilateral internal iliac artery ligation because of aneurysmal disease. One aortobifemoral-graft limb necessitated thrombectomy, but no cases of massive peripheral embolization occurred. When paraplegia was suspected after operation (6 to 20 hours after surgery), five patients underwent lumbar drainage. No clinical improvement was noted. CONCLUSION: Interference with pelvic blood supply from prolonged aortic cross clamping, intraoperative hypotension, aortic embolization, and interruption of internal iliac artery circulation have all been suggested as possible causes of spinal cord ischemia. In this survey, none of these factors proved to be significant as the sole cause of spinal cord ischemia. In the performance of an aortic operation with an end-to-end proximal anastomosis in the presence of severe external or internal iliac artery disease, there may be an increased incidence of spinal cord ischemia despite appropriate surgical techniques to ensure internal iliac perfusion. Spinal cord ischemia after abdominal aortic operations appears to be a tragically unpredictable, random, and unpreventable event. (+info)
Progressive myelopathy caused by dural arteriovenous fistula at the craniocervical junction--case report.
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A 68-year-old male presented an unusual dural arteriovenous fistula (AVF) located at the craniocervical junction. Magnetic resonance imaging revealed dilated perimedullary veins around the spinal cord at C-1 and C-2 levels, as well as high intensity signals in the spinal cord on T2-weighted images. Vertebral angiography identified an AVF at the point where the right vertebral artery penetrates the dura. The fistula was a single and direct communication between the vertebral artery and the spinal vein. Surgical interruption of the fistula at its venous side resulted in prompt improvement of both motor and sensory signs and symptoms. (+info)
Diffusion-weighted MRI in acute lacunar syndromes. A clinical-radiological correlation study.
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BACKGROUND AND PURPOSE: Clinical-radiological correlation studies in lacunar syndromes have been handicapped by the low sensitivity of CT and standard MRI for acute small-vessel infarction and their difficulty in differentiating between acute and chronic lesions. METHODS: We prospectively studied 43 patients presenting with a classic lacunar syndrome using diffusion-weighted MRI, a technique with a high sensitivity and specificity for acute small-vessel infarction. RESULTS: All patients were scanned within 6 days of stroke onset. An acute infarction was identified in all patients. Pure motor stroke was associated with lesions in the posterior limb of the internal capsule (PLIC), pons, corona radiata, and medial medulla; ataxic hemipareses with lesions in the PLIC, corona radiata, pons, and insular cortex; sensorimotor stroke with lesions in the PLIC and lateral medulla; dysarthria-clumsy hand syndrome with lesions in the PLIC and caudate nucleus; and pure sensory stroke with a lesion in the thalamus. Supratentorial lesions extended into neighboring anatomic structures in 48% of the patients. CONCLUSIONS: Lacunar syndromes can be caused by lesions in a variety of locations, and specific locations can cause a variety of lacunar syndromes. Extension of lesions into neighboring structures in patients with lacunar syndromes appears to be more frequent than previously described in studies using CT and standard MRI. (+info)
The clinical and epidemiological profile of tick-borne encephalitis in southern Germany 1994-98: a prospective study of 656 patients.
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Seven hundred and nine patients fell ill in southern Germany (Baden-Wurttemberg) after infection with the tick-borne encephalitis (TBE) virus between 1994 and 1998. Detailed clinical and epidemiological data on TBE were available for 656 patients. A biphasic course of the disease occurred in 485 patients (74%). TBE presented as meningitis in 320 patients (49%), as meningoencephalitis in 270 (41%) and as meningoencephalomyelitis in 66 (10%). Eight of the patients (1.2%) died from TBE. Four hundred and forty-five patients (68%) had noticed a tick bite and the first symptoms occurred, on average, 7 days later. The most frequent neurological symptoms were impairment of consciousness (31%), ataxia (18%) and paresis of the extremities (15%) and cranial nerves (11%). Laboratory investigations revealed leucocytosis in the peripheral blood in 224 out of 392 patients (74%), elevation of the erythrocyte sedimentation rate in 223 out of 245 (91%), increased C-reactive protein in 127 out of 155 (82%), pleocytosis in the CSF of all patients tested, damage of the blood-CSF barrier in 255 out of 322 (79%), abnormalities in EEG in 165 out of 214 (77%) and abnormalities in MRI in 18 out of 102 (18%). In general, adolescents up to 14 years of age had a more favourable course of the disease than adults. Of 230 patients who were re-examined at a later time, 53 (23%) had moderate or severe sequelae. Patients with sequelae presented more frequently (P < 0.001) with impaired consciousness (Glasgow Coma Scale < 7), ataxia, pareses of the extremities or cranial nerves, a need for assisted ventilation, abnormal findings in MRI, pleocytosis > 300 cells/microl and impairment of the blood-CSF barrier (total protein > 600 mg/l). In view of the severity of the illness and the high frequency of sequelae, active immunization against TBE is recommended for all subjects living in and travelling to areas of risk. Prevention of TBE by post-exposure prophylaxis with hyperimmunoglobulins is less effective and therefore should be performed only when absolutely necessary. (+info)
Recurrent spontaneous intracerebral hemorrhage in a congenitally afibrinogenemic patient: diagnostic pitfalls and therapeutic options.
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BACKGROUND: Coagulation disorders can cause intracerebral bleeding that may be difficult to detect since subsequent aberrant clot formation may mask early detection. This is an important pitfall because, when diagnosed early, bleeding in these patients is treatable. CASE DESCRIPTION: A patient with congenital afibrinogenemia presented with recurrent hemiparesis. Spontaneous intracerebral hemorrhage was diagnosed, despite an initial negative CT scan. Diagnosis, therapy, and complications of therapy are discussed. CONCLUSIONS: Intracerebral hemorrhage must be strongly suspected in any patient with a coagulation disorder presenting with matching clinical symptoms. Therapy must be installed immediately, before additional investigations, and should be continued even when initial neuroimaging is negative. (+info)