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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The subcortical arteriosclerotic encephalopathy of Binswanger is characterized clinically by hypertension, dementia, spasticity, syncope, and seizures. It is usually diagnosed pathologically by the finding in white matter of diffuse demyelination or foci of necrosis plus arteriosclerotic and hypertensive vasculopathy. We present a case in which the diagnosis was made on the basis of the clinical course and a computerized tomogram which demonstrated extensive white matter degeneration. Postmortem examination confirmed both the diagnosis and the extent of the degeneration as shown by CT scan.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger): computerized tomography. 57 97

Even in patients with complete loss of sensation and paraplegia after cervical spinal trauma, abdominal operations usually require general or spinal anesthesia due to spasms and increased muscle tone. Both anesthetic types have serious drawbacks under these circumstances, e.g. hyperkalemia induced by relaxation or the impossibility of adequate monitoring of the level of spinal blockade. After an onset time of 1-2 h the intrathecal injection of approx. 100 micrograms baclofen, a spinally acting GABAB-agonist, led to complete and long-lasting suppression of surgically induced spasticity. This could be demonstrated by neurological examination (spasticity scores: Ashworth score, spasm score, clonus score) during 5 neurosurgical operations in 3 patients with paraplegia. Except for slight sedation, the patients had no discomfort during operation. Intrathecal baclofen was also effective against autonomic hyperreflexia, i.e. vegetative dysregulation such as bradycardia or hypertension, provoked by catheterization or bladder surgery.
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PMID:[Intraoperative suppression of spasticity using intrathecal baclofen]. 230 48

Nine children treated for acute leukemia or lymphosarcoma developed subacute encephalopathy starting with listlessness, depression and impairment of speech. Walking difficulties, ataxia, spasticity and sphincter disorders developed later. Transient intracranial hypertension and abnormal movements respectively developed in two patients. EEG frontal slow waves, raised CSF protein, abnormal white matter radioisotope uptake and CT scan hypodensity with patchy contrast enhancement were evident at the onset. Later, dilated ventricles and calcification appeared in the younger patients. Post-mortem neuropathological studies of three patients disclosed predominantly perivascular myelin loss in areas of white matter necrosis, abnormalities of small vessels and numerous axonal swellings. The spinal cord showed secondary degeneration of the corticospinal tracts. Analysis of the aetiological factors in this series points to the prevailing danger of cranial radiotherapy, probably increased by the young age of patients and by associated drug administration.
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PMID:Necrotising leukoencephalopathy complicating treatment of childhood leukaemia. 669 15

Sixty-five cases of clinically diagnosed multiple lacunar state have been analysed. The clinical course of multiple lacunar state is usually progressive in nature, simulating degenerative diseases, in contrast with the mode of acute onset seen in the other vascular diseases. Average age at the initial visit was 63.8 year-old, and sex ratio showed marked male preponderance, being 12 for males and 1 for females. Gait disturbance and speech disturbance are the most frequent initial symptoms, followed by slow motion, emotional lability and swallowing difficulty. Neurological manifestations are dysarthria, short-stepped and apraxic gait, hyperreflexia, positive Babinski and Chaddock reflexes, minimal spasticity, dementia, positive palmo-mental reflex, emotional lability, fixed face, rigidity, bradykinesia, foot grasping, dysphagia, positive Myerson's sign and tremor, in the order described. The important point is that the rigidity is paratonic and the tremor is action or postural, not the cogwheel rigidity or resting tremor like Parkinson's disease. The appearance of pathological reflexes (Babinski and Chaddock reflexes) are quite important, especially Chaddock reflex, which can frequently become positive despite negative or equivocal Babinski reflex. Hypertension, especially longstanding in nature, is the major contributing factor in this disorder. CT scan showed the presence of one or more lacunes in 52 out of 65 cases (80.0%). The detection of lacune can be influenced by the quality of CT scan, and the high resolution CT scanner is greatly useful for that purpose. It is stressed that the detailed neurological and computed tomographic evaluations will make it possible to reach the clinical diagnosis and appropriate treatment of multiple lacunar state.
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PMID:[Clinical studies on multiple lacunar state]. 674 15

Pregnancy in a patient suffering from high spinal cord lesions is unusual and can lead to serious autonomic hyperreflexia during delivery. Epidural anaesthesia has been suggested as a means of decreasing such a risk. This clinical report presents the case of a paraplegic patient with lesions above the T3 level who had spinal anaesthesia for a Caesarean section. Her first delivery, six years earlier and without spinal anaesthesia was complicated by serious autonomic hyperreflexia with severe hypertension, seizures and inhalation. These symptoms were at first interpreted as eclampsia. For the Caesarean section, spinal anaesthesia using 0.25% bupivacaine in divided doses presented no difficulty, in spite of important lordosis, and permitted the delivery of a newborn with an Apgar score of 10 at one minute. The upper sympathetic level reached (T4-T6) was assessed by the discontinuing of muscular spasticity and contractures elicited by cutaneous stimuli. At the present time, spinal anaesthesia is the best method for preventing autonomic hyperreflexia. General anaesthesia, especially with halothane, is effective, but requires a deeper anaesthesia with the risk of serious hypotension and its possible repercussions on the fetus. Moreover it does not decrease the risk of autonomic hyperreflexia during the postoperative period.
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PMID:[Epidural anesthesia and prevention of autonomic hyperreflexia in a paraplegic parturient]. 831 56

Three children with pronounced livedo reticularis present since birth (cutis marmorata-telangiectasia congenita) have been followed to the ages of eight, 17 and 21 years. During childhood they developed frequent recurrent transient stroke-like hemipareses, affecting either side of the body, associated with ipsilateral pain, headache, visual symptoms, dysphasia, fits and confusion. Intellectual failure and, in one, progressive spasticity have followed. Attacks were more frequent in winter. Other problems have included abnormal peripheral vascular responses to temperature change, gastro-intestinal bleeding, glaucoma, local tissue hypertrophy and, in the two older patients, renal involvement with hypertension. Their condition represents a form of congenital vasculopathy. Anticonvulsants, anti-migraine agents, anti-platelet drugs and flunarizine have been ineffective. Nifedipine prevented further attacks in one patient and reduced attacks in another, but has not helped the third child. Adequate clothing and warmth may also be important.
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PMID:Congenital livedo reticularis and recurrent stroke-like episodes. 840 21

As alluded to at the onset, our purpose is to provide a periodic reminder about autonomic dysreflexia/hyperreflexia (AD). Some historical background was offered since so much of the recent literature has been obtained from Medline which started in 1966. There were a number of early pioneers who first labored with AD. Kewalramani, in his fine paper, found various names for AD in the literature: sympathetic hyperreflexia, paroxysmal hypertension, spinal poikilopiesis, autonomic spasticity, paroxysmal hyperactive autonomic reflexes and paroxysmal neurogenic hypertension. Why not use only one term for this life threatening syndrome: autonomic dysreflexia/hyperreflexia.
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PMID:Autonomic dysreflexia/hyperreflexia. 926 82

After spinal cord injury, hyper-reflexia can lead to episodic hypertension, muscle spasticity and urinary bladder dyssynergia. This condition may be caused by primary afferent fiber sprouting providing new input to partially denervated spinal interneurons, autonomic neurons and motor neurons. However, conflicting reports concerning afferent neurite sprouting after cord injury do not provide adequate information to associate sprouting with hyper-reflexia. Therefore, we studied the effect of mid-thoracic spinal cord transection on central projections of sensory neurons, quantified by area measurements. The area of myelinated afferent arbors, immunolabeled by cholera toxin B, was greater in laminae I-V in lumbar, but not thoracic cord, by one week after cord transection. Changes in small sensory neurons and their unmyelinated fibers, immunolabeled for calcitonin gene-related peptide, were assessed in the cord and in dorsal root ganglia. The area of calcitonin gene-related peptide-immunoreactive fibers in laminae III-V increased in all cord segments at two weeks after cord transection, but not at one week. Numbers of sensory neurons immunoreactive for calcitonin gene-related peptide were unchanged, suggesting that the increased area of immunoreactivity reflected sprouting rather than peptide up-regulation. Immunoreactive fibers in the lateral horn increased only above the lesion and in lumbar segments at two weeks after cord transection. They were not continuous with dorsal horn fibers, suggesting that they were not primary afferent fibers. Using the fluorescent tracer DiI to label afferent fibers, an increase in area could be seen in Clarke's nucleus caudal to the injury two weeks after transection. In conclusion, site- and time-dependent sprouting of myelinated and unmyelinated primary afferent fibers, and possibly interneurons, occurred after spinal cord transection. Afferent fiber sprouting did not reach autonomic or motor neurons directly, but may cause hyper-reflexia by increasing inputs to interneurons.
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PMID:Sprouting of primary afferent fibers after spinal cord transection in the rat. 962 43

Major neurologic complications secondary to cyclosporine are well documented and are known to include confusion, cortical blindness, seizure, spasticity, paresis, ataxia and coma. Most previous reports attribute these to white matter central nervous system (CNS) lesions or white/grey matter border lesions. Many predisposing factors have been identified, including: elevated levels of cyclosporine, hypomagnesemia, hypocholesterolemia, aluminium toxicity, high dose steroids, hypertension and infection. However CNS events attributed to cyclosporine have been reported without any of these risk factors. We report a case of a child developing multiple white and grey matter thalamic and cortical lesions along with acute neurologic deterioration, and then review cyclosporine mediated CNS injury, including the roles of P-glycoprotein and cyclophilin.
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PMID:Cyclosporine-induced white and grey matter central nervous system lesions in a pediatric renal transplant patient. 1008 60

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80


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