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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since 1978, the authors have observed 7 cases of dissecting aneurysm in the internal carotid artery. Symptoms were severe headache and subsequent neurologic deficit in young persons (3 women, 4 men; mean age 35 years). The underlying pathology was spontaneous dissection of the cervical internal carotid artery, with surgical confirmation in 3 cases and typical angiographic patterns in all cases. Spontaneous dissection of the cervical internal carotid artery is being increasingly recognized as a cause of cerebral ischemia in young adults. Moreover this clinicopathologic event is more common than had previously been supposed. The etiology remains unclear, except in 15% of cases in which dystrophy of the media (Marfan's syndrome) is in cause. No history of cervical trauma can be found. Typical clinical features consist in ipsilateral headache preceding an abrupt neurologic deficit in a 40-year-old person. An incomplete Horner syndrome (oculosympathetic paresis without facial anhidrosis) associated with facial pain and numbness is pathognomonic, but the majority of dissections are less typical. The typical angiographic pattern is an elongated regular stenosis of the high cervical internal carotid artery, 2 cm above the non-involved bulbus ("string sign"). The dissection may modify to a tapered occlusion above the point of origin of the internal carotid artery. The natural course is spontaneous resolution of the stricture, without relapse. Optimal management is non-operative since medical treatment has proved to be efficient. These cases confirm the benign course and overall good prognosis of spontaneous dissections of the internal carotid artery which are not as rare as the scarcity of reports might indicate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous dissection of the internal carotid artery. Apropos of 7 cases and a review of the literature]. 217 45

Noniatrogenic traumatic extracranial internal carotid artery dissections were encountered in six patients (five men and one woman) 31 to 62 years old. All but one had overt cerebral ischemia manifest by paresis (three), sensory deficits (three), aphasia (three), or amaurosis fugax (two), One patient had an asymptomatic carotid artery bruit. Cerebral arteriography established the diagnosis in all cases. Internal carotid artery impingement between the mandible and transverse processes of the second and third cervical vertebrae, or undue stretching over these vertebral structures, were the most likely primary mechanisms of injury. Secondary complications, a result of distal thromboembolism, were evident in two patients. Direct cerebral revascularization, staged internal carotid artery constriction and ligation, as well as intensive nonoperative therapy were valid therapeutic options. There were no deaths. Treatment relieved transient ischemic symptoms or arrested progression of established neurologic deficits in each case. In select patients, early surgical intervention may lessen attending neurologic sequelae.
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PMID:Extracranial internal carotid artery dissections: noniatrogenic traumatic lesions. 706 89

Infusions of 5% albumin and/or dextran 40 in nine patients with acute ischemic neurological deficits reduced mean hematocrit values from 41% to 32%, raised mean central venous pressure from 4 to 12 cm H2O, and reduced mean arterial BP from 101 to 94 mm Hg. Six alert patients had ischemic structural damage on cranial computed tomography. All six alert patients with upper arm paresis objectively improved and two others with only dysphasia also improved within 24 hours after infusion initiation. Although the improvement in two patients seemed to be temporarily dependent on the continuing of the infusion, all eight alert patients were eventually weaned without loss of regained function. This report of neurological improvement during hypervolemic hemodilution suggests that augmentation of collateral perfusion secondary to reduced blood viscosity may rapidly relieve cerebral ischemia, impede infarction, and allow time for compensatory mechanisms to maintain blood flow above ischemic thresholds.
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PMID:Observations during hypervolemic hemodilution of patients with acute focal cerebral ischemia. 714 73

Aneurysms of the extracranial internal carotid artery are rare but can be responsible for severe complications such as rupture, thrombosis, or embolism. Between 1961 and 1985 we operated on 38 aneurysms of the extracranial internal carotid artery in 35 patients, 22 males and 13 females, whose ages ranged from 6 to 73 years. The underlying causes of aneurysm included atherosclerosis (12 cases), fibromuscular dysplasia (eight cases), a congenital defect (five cases), infection (one case), and trauma (six cases); in six cases aneurysm was secondary to spontaneous dissection. Signs of cerebral ischemia were present in 26 (74%) patients and a cervical mass was found in six. The aneurysm was proximal (i.e., below the angle of the mandible) in 16 patients and distal (i.e., above the angle of the mandible) in 22. After resection of the aneurysm, arterial continuity was restored in 37 patients by resection and grafting (12 cases), resection and anastomosis (11 cases), or arteriorrhaphy (14 cases). One death occurred 13 days after operation due to myocardial infarction. Two patients experienced a reversible neurologic event. Transient paresis of cranial nerves was observed in eight patients. During a follow-up period that ranged from 6 to 30 years, four patients were lost to follow-up and 25 patients remained asymptomatic. Three patients had asymptomatic thrombosis of the carotid artery detected at follow-up investigations. The potential risks of cerebral ischemia and rupture and the satisfactory long-term results achieved with surgery are strong arguments in favor of surgical treatment for aneurysms of the extracranial internal carotid artery.
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PMID:Surgical treatment of extracranial internal carotid artery aneurysm. 781 77

A study was performed to compare the follow-up results of superficial temporal artery-middle cerebral artery anastomosis between a group of nine elderly patients (aged 70 years or over) and another group of 24 non-elderly patients (aged less than 70 years) with cerebral ischemia. The 33 patients, comprising 26 males and seven females, were evaluated pre- and postoperatively by four-vessel angiography, CT scan, MRI and cerebral blood flow (CBF) examination using either xenon inhalation or 123I-IMP SPECT. In some patients, additional evaluations were done. For those with dementia, the minimental scale (MMS), P300 event-related potential, the Hachinski ischemia score, and the vowel word counting test (Kaneko's KANAHIROI) were used, and for the hemiplegic, the Barthel index indicating ability of daily life (ADL) was employed. The results of follow-up for periods ranging from 12 to 55 months were "excellent" (returned to previous job) or "good" (able to perform self-care) in 27 of the 33 patients (81.8%) including six (66.6%) of the elderly group and 21 (87.5%) of the non-elderly group. There was no significant difference between the two groups by statistical evaluation. Among the nine patients with dementia (five under 70, four 70 years of age or over), eight (four under 70, four 70 or over) showed "rapid recovery" with improved postoperative MMS, P300, vowel word counting score and CBF. One patient under 70 (Case 5; a 47-year-old male) with a delayed 2-day recovery from general anesthesia, took as long as 6 months to obtain the self-care ability in daily life. Excluding this patient, all of the remaining eight patients responded quickly to surgery and were able to go home with their families after 2 to 4 weeks, there being no significant difference between the two age groups. In the 14 patients with hemiplegia/paresis (nine under 70, five 70 or over), a definitely better result was obtained for the non-elderly group. Eight of the nine non-elderly patients (89%) showed full ADL (Barthel index 100), whereas only one of three elderly patients (33.3%) showed almost full ADL (Barthel index 97). In five progressive stroke patients, (three under 70, two 70 or over) ultra-early bypass was performed within 8 hours postictus. Definitely better results were obtained in the patients aged less than 70, who showed rapid recovery and were able to return to their previous jobs 1 to 3 months after surgery. In contrast, the two patients aged 70 or over showed no improvement. In this report, we discuss the clinical and physiological variables that may be important for selection of elderly patients for cerebrovascular bypass surgery.
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PMID:[Results of superficial temporal artery-middle cerebral artery anastomosis for elderly and non-elderly patients with cerebral ischemia]. 782 13

In muscles with sustained voluntary contraction, EMG activity is transiently inhibited after transcranial magnetic stimulation. We recorded this postexcitatory silent period (SP) at 1.5 times individual stimulus threshold level from the first dorsal interosseus muscle in 65 neurologic patients aged 11 to 80 years. When compared with 20 healthy volunteers and a subgroup of patients with peripheral neurologic conditions not affecting the tested pathways, the SP was significantly longer on the paretic side in cerebral ischemia (p < 0.001) and chronic inflammatory CNS diseases, such as multiple sclerosis or neurosarcoidosis (p < 0.01). There was a similar tendency in pyramidal tract lesions due to CNS tumors and spinal cord trauma. In lesser degrees of paresis, SP duration is more sensitive than central motor conduction time (CMCT), but its specificity awaits further evaluation. SP is dependent on the integration of motor excitatory and inhibitory pathways and, possibly, sensorimotor reflex systems. In contrast to SP duration, which proved to be an independent variable giving supplementary information over the usual CMCT measurement, SP onset latency correlates well with CMCT and peripheral nerve conduction slowing, as in polyradiculoneuritis.
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PMID:Latency and duration of the muscle silent period following transcranial magnetic stimulation in multiple sclerosis, cerebral ischemia, and other upper motoneuron lesions. 819 Mar

Four patients presented with hemiballism-hemichorea as a clinical manifestation of white matter ischemia. These patients illustrate "positive" motor phenomena rather than limb weakness as a consequence of cerebral ischemia. In each patient, the involuntary movements disappeared following worsening of paresis. Subcortical white matter infarction in three patients and hemodynamic hypo-perfusion in the cerebral hemisphere contralateral to dyskinetic movements were possible causes. Neuroradiologically, none had pathological changes in the vicinity of the subthalamic nucleus. We presume from these observations that ischemia of the subcortical white matter, without involvement of the basal ganglia or the subthalamic nucleus, may cause hemiballism-hemichorea.
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PMID:Hemiballism-hemichorea induced by subcortical ischemia. 831 49

In order to evaluate the effectiveness of acute cerebral revascularisation, we conducted a review of 70 patients with acute arterial occlusion or severe stenosis. Of these, 35 underwent emergency superficial temporal artery--middle cerebral artery (STA-MCA) anastomosis (surgical group) and the other 35 were treated conservatively (non-surgical group) at different times. Statistical analysis indicated that the two groups were homogeneous for the prognostic indicators. Seven days after admission, neurological symptoms and signs improved in 43% of patients in the surgical group and in 29% of the non-surgical group, however, this difference was not significant. The ratios of independent life at 3 months were 51% and 31%, respectively (not significant). Subgroup analyses indicated that final outcomes for patients with mild to moderate paresis on admission were significantly better in the surgical group than in the non-surgical group (94% vs. 53%, p < 0.01). The ratios of haemorrhagic infarction, neurological worsening, and mortality were comparable between the two groups. Time of ischaemia is a less important factor in the criteria for surgical selection. Acute revascularisation in selected patients does improve a natural course and could be a therapeutic option for acute cerebral ischaemia.
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PMID:Superficial temporal artery--middle cerebral artery anastomosis for acute cerebral ischemia: the effect of small augmentation of blood flow. 878 52

Cerebral hypoxia is a major component of immediate and secondary cell damage caused by ischemia. Hyperbaric oxygen (HBO) is a potent means to increase the amount of oxygen dissolved in blood plasma. The effectiveness of HBO in clinical and experimental cerebral ischemia, however, is controversial. We sought to determine whether treatment with HBO initiated early after focal cerebral ischemia-onset protects the brain when experimental conditions such as brain temperature are controlled. Male Wistar rats (n=57) underwent reversible filament occlusion of the right middle cerebral artery (MCA) for 75 min. Animals were awakened after filament introduction and assessed for presence of forelimb paresis. Rats then underwent a 60-min course of either 100% O(2) at 1.0 atmosphere absolute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiological monitoring and pericranial temperature control. The filament was then removed. Seven days after ischemia, rat behavior was scored from 3-18 (18=normal) and brains were removed for histological analysis of infarct volume. Rats treated with HBO 2.5 ata had better mean+/-standard deviation (S.D.) behavioral scores (14+/-2; p<0.05) than control (10+/-3) or HBO 1.5-ata-treated animals (11+/-3). Similarly, total infarct volumes (mean+/-S.D.) were smaller in animals receiving HBO at 2.5 ata (76+/-65 mm(3); p<0.05) compared to control (129+/-83 mm(3)) and HBO 1.5-ata (119+/-68 mm(3))-treated groups. Cortical infarction occurred less frequently in HBO 2. 5-ata-treated than in control animals (44% vs. 71%; p<0.05). We conclude that HBO can improve outcome after temporary focal ischemia when treatment is started early after ischemia-onset but HBO dose appears important. Potential mechanisms include enhanced oxygen supply to marginally perfused cells.
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PMID:Hyperbaric oxygen decreases infarct size and behavioral deficit after transient focal cerebral ischemia in rats. 1062 9

Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.
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PMID:Spontaneous carotid dissection presenting lower cranial nerve palsies. 1123 57


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