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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The somatosensory abnormalities in 20 men and 7 women (mean age 67 years, range 53-81) with central post-stroke pain (CPSP) have been analysed in detail with traditional neurological tests and quantitative methods. The cerebrovascular lesions were located in the lower brain-stem in 8 patients, involved the thalamus in 9 and in 6 were suprathalamic. In 4 patients the location of the CVL could not be determined. All patients had abnormal temperature and pain sensibility, with a severe deficit in most cases. All except 2 had raised thresholds to thermal pain and all except 1 had abnormal sensibility to pin-prick. Eighty-eight percent exhibited hyperpathia with combined loss and suprathreshold exaggeration of somatic sensibility. In 85% somatic stimuli evoked dysaesthesia and about half of these patients also experienced spontaneous dysaesthesia. Paraesthesias were reported by 41%, radiation of stimuli by 50%, after-sensations by 45% and allodynia by 23%. Vibration sensibility was abnormal in 41%; raised thresholds to the perception of touch were found in 52%, to 2-PD in 35%, to dermolexia in 45% and to joint movements in 37%. The results indicate that all patients with CPSP have lesions that affect the major pathways for temperature and pain sensibility, i.e., the spino-thalamo-cortical pathways. Furthermore it appears that neither the level of the lesion along the neuraxis nor concomitant injury to the medial lemniscal pathways is crucial for the development of CPSP. The results confirm the notion that CPSP is a deafferentation syndrome, but they also provide evidence against the hypothesis that CPSP is a release phenomenon caused by a lesion that removes inhibitory influences of the lemniscal pathways on neurones that evoke pain.
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PMID:Central post-stroke pain--a study of the mechanisms through analyses of the sensory abnormalities. 274 90

Etiological factors and clinical course of transient disorders of the cerebral circulation developing at various terms of gestation and in the immediate postpartum period were studied in 132 women. Early symptoms of a cerebral crisis included headache, vertigo, palpitation, dyspnea, darkness in the eyes, noise in the ears or head, paresthesia, and numbness of the legs. Occasionally, it had to be differentiated from a cerebral stroke. The most important etiological factors of this cerebrovascular pathology included toxemia of pregnancy, exacerbation of the rheumatic process, essential hypertension, vegetovascular dystonia, intracranial aneurysm, etc. Various combinations of a number of etiological factors of transient disorders of the cerebral circulation are possible. Recommendations about the management of pregnancy and parturition are offered.
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PMID:[Transient cerebral circulatory disorder in pregnant women]. 342 70

An unusual case of mandibular paresthesia as the only presenting symptom of a cerebrovascular accident is presented. The differential diagnosis of inferior alveolar nerve paresthesia is discussed. Obtaining a definitive diagnosis depends on a thorough medical and dental history complemented by a complete clinical and radiographic examination. The etiology of cerebral vascular accidents is reviewed, as well as risk factors that may increase the possibility of a cerebrovascular accident.
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PMID:Mandibular paresthesia secondary to cerebrovascular changes. 346 4

In 1980, 120 cases with late-life migrainous accompaniments resembling transient ischemic attacks were presented. In the present paper, 85 further cases examined in the past five years are analyzed. The findings support the concept advanced previously. In general, the cases are divided into the same categories: visual--21 cases, visual and paresthesias--6, visual and speech disturbance--2, visual, paresthesias and speech disturbance--3, visual, paresthesias, speech disturbance, and weakness--20, visual and brainstem symptoms--3, and cases without visual symptoms--32. The ages ranged from 40 to 73 years. Headache occurred in association with the episodes in only 40% of cases. There was a history of recurrent headache in 65%. The condition can justifiably be regarded as benign. Migrainous accompaniments account for some of the cases of transient ischemia with normal angiograms. Knowledge of the condition helps in the planning of rational management.
Stroke
PMID:Late-life migraine accompaniments--further experience. 353 32

Migraine headaches that occur in the 15- to 30-year-old age group are well documented. In patients in the stroke age bracket, however, who present with a history of neurologic deficit, transient ischemic attacks can be confused with migraine accompaniments. The typical patient is 50 years old, is without a past history of migraines, and complains of scintillating visual disturbances (20 percent), marching paresthesis (22 percent), or a myriad of neurologic deficits. In one series of 70 neurology patients aged over 55 years, 16 percent reported that they experience the new onset of scintillations. Once fully evaluated, the cause of unexplained marching paresthesias, dysphagia, or hemiplegia, once reserved for thrombotic or embolic phenomena, may be attributed to migraine accompaniments. In the face of a normal evaluation, neurologic deficit in the stroke age bracket may be attributed to migraine accompaniments. A case of a 47-year-old woman with sudden onset of left-sided paresthesia, dysarthria, and confusion is presented. The discussion includes a description of migraine pathophysiology and a review of concepts regarding accompaniments.
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PMID:Late-life migraine accompaniments: a case presentation and literature review. 358 61

This paper contains an analysis of 135 cases in which numbness, either episodic or persistent, involved one side of the body. In most cases, the patients were candidates for the diagnosis of pure sensory stroke which is usually the result of an occlusive cerebrovascular lesion involving the thalamus. The cases are divided into three main categories, pure sensory stroke, pure sensory TIAs, and atypical cases. The clinical features described in an earlier paper have been confirmed for the most part. A major limitation is the paucity of pathological studies. The lack of reliable criteria for the recognition of migrainous paresthesias has probably resulted in the inadvertent inclusion of some such cases. Some other conditions, hemidysesthesia and cervical disc, which have had to be considered in the differential diagnosis have been included. Cases of occlusive disease of the posterior cerebral internal carotid and middle cerebral arteries have been analyzed for patterns of paresthesias which may serve to distinguish cortical lesions from thalamic.
Stroke
PMID:Pure sensory stroke and allied conditions. 710 42

3 case studies of migrainous patients taking oral contraceptives (OCs) are presented in this report. The role of OCs in triggering a migraine attack and possibly elevating the risk of a stroke in a patient with migraines is examined. In the 1st case, a 27-year old white female accountant complained of temporal throbbing headaches associated with nausea, vomiting, hazy vision, small scotomas, and photophobia. The patient had been having the headaches twice a month since 1978 and she took Fiorinal to relieve them. Her physician diagnosed the headaches as migraine. The patient acknowledged that she started getting these headaches after beginning to use OCs 3 years earlier. Her family history revealed that her mother had severe migraine headaches which sometimes were accompanied by unilaterial paresthesia, as well as high blood pressure. Ophthalmoscopy, slitlamp, accommodation, and intraocular pressure findings were unremarkable. The patient was counseled about the factors which can trigger a migraine attack and was advised that eliminating these factors may reduce the frequency and intensity of the headaches. The patient was advised that OCs could increase her risk of having a stroke, especially with her family history. Her family physician subsequently reduced the dosage of her OCs. 5 months later the patient reported that she was trying to avoid the migraine triggering factors (e.g., she was wearing her sunglasses). Her headaches had become less frequent and less severe. The 2nd patient also began to have migraine attacks after beginning to use OCs. The 3rd patient's headaches became so severe after taking the pill that she consulted a neurologist. The 2nd and 3rd patients complained that the headaches were most severe at the time each month when they resumed OC use. None of the 3 patients discontinued OC use. The 2nd and 3rd patients were using a low estrogen OC, and the 1st patient was put on a low estrogen dosage after this optometrist's recommendation to her physician. Encouraging the patients to discuss the dosage of OCs with their family physician may be one of the ways to reduce the unwanted effect of the pill. The effect of OCs goes beyond triggering a headache. They may trigger a stroke particularly if the patient has a family history of high blood pressure as did the patients in this study. Differential diagnosis of migraine headaches includes muscle contraction, tension, sinus, and allergic headaches. Optometrists can be most helpful to the patients by counseling them to avoid the triggering factors. Glare, a triggering factor, could be reduced by tinted spectacles.
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PMID:Migraine and oral contraceptives. 714 75

Occasionally patients in the stroke age-bracket over 40 have unexplained transient cerebral ischemic attacks in association with normal cerebral angiograms. From this group 120 have been collected in whom the transient episodes resembled the neurological accompaniments of migraine. According to symptoms, the patients were categorized as follows: Visual accompaniments (patients with only ordinary scintillating scotoma were excluded), 25; visual and paresthesias, 18; visual and speech disturbance, 7; visual, and brain stem symptoms, 14; visual, paresthesias, and speech disturbance, 7; visual, paresthesias, speech disturbance and paresis, 25; recurrence of old stroke deficit, 9; miscellaneous, 8. In establishing the diagnosis angiography is advisable in all but classical cases. Typical of migrainous accompaniments are the buildup and migration of visual scintillations, the march of paresthesiae, and progression from one accompaniment to another, characteristics that do not occur in thrombosis and embolism. Diagnosis facilitated when 2 or more similar episodes have occurred or migraine-like scintillations are present. Headache occurred in 50% of cases. Other cerebrovascular processes, coagulation disorders, and cerebral seizures must be ruled out.
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PMID:Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks. 738 4

The high affinity noncompetitive N-methyl-D-aspartate receptor antagonist CNS 1102 (aptiganel hydrochloride, Cambridge NeuroScience, Cambridge, MA.) is neuroprotective in preclinical models of stroke when administered as pretreatment or up to 60 minutes postischemia, and has potential for treatment of acute stroke or traumatic brain injury in man. A total of 55 healthy male subjects have participated in three separate studies to determine the clinical pharmacology of CNS 1102, 43 of whom have received CNS 1102 in doses of up to 100 micrograms/kg. Administration of CNS 1102 has been studied as a 15-minute intravenous infusion, as a 15-minute loading intravenous infusion followed by a 4-hour maintenance infusion, or as a fixed-dose intravenous bolus over 90 seconds. CNS 1102 in normal volunteers is well tolerated in total doses up to 32 micrograms/kg whether as a bolus injection, 15-minute infusion or 4-hour infusion. Central nervous system affects are evident within minutes of administration, implying rapid drug penetration. CNS 1102 has a large and variable volume of distribution (mean +/- standard deviation, 6.2 +/- 1.9 l/kg), variable clearance (115 +/- 77 l/h), and plasma half-life of approximately 4.5 hours. Adjustment of doses by subject weight does not improve variability of these parameters, and fixed doses may thus be administered. CNS 1102 causes dose-dependent elevation of blood pressure, accompanied by clinical evidence of vasoconstriction. Global cerebral blood flow is maintained, whilst middle cerebral artery flow velocity increases. Symptoms of light-headedness, disorientation and paresthesia progress through euphoria, disinhibition, and hallucinations to psychomotor retardation, paranoia and catatonia as total administered dose increases.
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PMID:Clinical pharmacology of CNS 1102 in volunteers. 748 14

Paresthesia-producing (PP), but not periventricular grey (PVG) deep brain stimulation (DBS) proved effective in steady neuropathic pain in 25 patients receiving both, regardless of the PP site stimulated, but PVG-DBS suppressed allodynia or hyperpathia in 3 cases of stroke-induced pain. In patients with stroke-induced central pain, PP-DBS was unpleasant in 6 of 17 (35%), all with allodynia and/or hyperpathia, but not in patients with spinal cord central or peripheral neuropathic pain with allodynia or hyperpathia. Of 11 patients in whom prior ineffective dorsal column stimulation (DCS) produced appropriate paresthesia, none responded to PP-DBS; 5 of 7 did so in whom DCS produced no paresthesia or relieved pain. Periaqueductal grey DBS was nearly always unpleasant, PVG-DBS sometimes was.
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PMID:Deep brain stimulation for neuropathic pain. 891 40


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