Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old man was admitted to our clinic because of the pain of left extremities for four years. The patient developed dysesthesia, hyperpathia and spontaneous pain 2 months after the onset of cerebrovascular accident with left hemiparesis. Using Toshiba TCT-20A CT scanner and Leksell's CT-stereotaxic system, stimulation electrode (by Medtronic Co.) was implanted in the posterior limb of the internal capsule which was 25 mm lateral to the posterior commissure. Ventriculography was not necessary because the target point was directly measured from the axial CT and midsagittal reformatted CT based on 18 axial CT images (2 mm thick slices). Anterior commissure, pineal calcification, posterior commissure and Sylvian aqueduct were demonstrated on the midsagittal reformatted CT by this method. The pain was relieved by the ramped square pulse stimulation (2 V, 0.6 msec, 50 Hz) and receivor system was internalized. The patient was free from pain by 30 minutes-long stimulation four to six times a day. Precise electrode placement was possible by CT images alone using high resolution CT and CT-stereotaxic system. CT-guided stereotaxic technique seemed to have an advantages especially for the implantation of electrode in the posterior limb of the internal capsule. The reason is as follows: The target is just lateral to the posterior commissure which could be recognized easily on the midsagittal reformatted CT. The internal capsule is advantageously demonstrated on the axial CT.
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PMID:[CT-guided stereotaxic implantation of a deep brain electrode for the stimulation of the internal capsule--a case report]. 351 39

Central post-stroke pain (CPSP) is a neuropathic pain syndrome characterized by constant or intermittent pain in a body part occurring after stroke and associated with sensory abnormalities in the painful body part. This study describes CPSP prospectively during the first year after stroke and characterizes the cerebrovascular lesions and neurological signs associated with the CPSP syndrome. Two hundred and sixty-seven consecutively admitted patients younger than 81 years were examined in the first week, at 1, 6 and 12 months after stroke. Sensibility to touch (cotton wool), temperature (20 degrees C and 40 degrees C), and pinprick was studied using the contralateral face and extremity as control. A CT scan was done 8 (median) days (range: 1-34 days) after stroke. Two hundred and seven (78%) patients surviving at least 6 months who were able to communicate reliably formed the basis of the study. Abnormal sensory signs were found at least once in 87 (42%) patients. CPSP was found in 16 (8%) patients of whom all but 1 patient also had evoked dysesthesia or allodynia. Further 1 patient had persistent evoked dysesthesia but denied pain. CPSP was not related to sex or age. In patients with single acute cerebral lesions there were no relation between size or location of the lesions and the presence of CPSP. The pain was light in 6 (3%) patients and moderate to severe in 10 (5%) patients. The pain quality was usually lacerating or aching. Fifteen (94%) patients had decreased temperature, touch and pain sensibility and 9 (56%) reported allodynia to cold stimulation and another 9 (56%) patients reported this to touch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence of central post-stroke pain. 765 28

The nucleus caudalis DREZ operation has been performed in three phases at Duke. Between 1982 and 1988 radiofrequency (RF) lesions were made in the trigeminal nucleus extending from the C2 root to the obex using a straight electrode. Complications include ipsilateral arm ataxia due to spinocerebellar tract injury and ipsilateral lower limb weakness from the pyramidal tract. The former occurred at least transiently in 90% of cases. The electrode employed from 1988 to 1989 had proximal insulation protecting the spinocerebellar tract. Since 1989 a ninety degree bend has been added to the electrode to allow better placement. Two electrodes are used to accommodate the shape of the caudalis nucleus. A total of 101 procedures have been performed. The newest electrodes were used in 46 procedures. Ataxia is recognized in 39%. Overall pain relief was excellent in 34% and good in 40%. In post herpetic neuralgia 71% enjoyed excellent or good relief. Indications include post herpetic neuralgia, deafferentation pain (anaesthesia dolorosa, post-tic dysesthesia, stroke, MS, gasserian tumour, Gamma Knife radiation injury), facial trauma/surgery, atypical facial pain, and migraine/cluster headache. A study to compare this operation to deep brain stimulation prospectively for the above indications has been initiated.
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PMID:The Duke experience with the nucleus caudalis DREZ operation. 874

Spasticity is a velocity-dependent increase in stretch reflex activity. It is one of the forms of muscle overactivity that may affect patients with damage to the central nervous system. Spasticity monitoring is relevant to function because the degree of spasticity may reflect the intensity of other disabling types of muscle overactivity, such as unwanted antagonistic co-contractions, permanent muscle activity in the absence of any stretch or volitional command (spastic dystonia), or inappropriate responses to cutaneous or vegetative inputs. In addition, spasticity, like other muscle overactivity, can cause muscle shortening, which is another significant source of disability. Finally, spasticity is the only form of muscle overactivity easily quantifiable at the bedside. Under the name pharmacological treatments of spasticity, we understand the use of agents designed to reduce all types of muscle overactivity, by reducing excitability of motor pathways, at the level of the central nervous system, the neuromuscular junctions, or the muscle. Pharmacologic treatment should be an adjunct to muscle lengthening and training of antagonists. Localized muscle overactivity of specific muscle groups is often seen in a number of common pathologies, including stroke and traumatic brain injury. In these cases, we favor the use of local treatments in those muscles where overactivity is most disabling, by injection into muscle (neuromuscular block) or close to the nerve supplying the muscle (perineural block). Two types of local agents have been used in addition to the newly emerged botulinum toxin: local anesthetics (lidocaine and congeners), with a fully reversible action of short duration, and alcohols (ethanol and phenol), with a longer duration of action. Local anesthetics block both afferent and efferent messages. The onset of action is within minutes and duration of action varies between one and several hours according to the agent used. Their use requires resuscitation equipment available close by. When a long-lasting blocking agent is being considered, we favor the use of transient blocks with local anesthetics for therapeutic tests or diagnostic procedures to answer the following questions: Can function be improved by the block? What are the roles played by overactivity and contracture in the impairment of function? Which muscle is contributing to pathologic posturing? What is the true level of performance of antagonistic muscles? A short-acting anesthetic can also serve as preparation to casting or as an analgesic for intramuscular injections of other antispastic treatment. Alcohol and phenol provide long-term chemical neurolysis through destruction of peripheral nerve. Experience with ethanol is more developed in children using intramuscular injection, while experience with phenol is greater in adults with perineural injection. In both cases, there are anecdotal reports of efficacy but studies have rarely been controlled. Side effects are numerous and include pain during injection, chronic dysesthesia and chronic pain, and episodes of local or regional vascular complications by vessel toxicity. In the absence of controlled studies, a theoretical comparison of neurolytic agents with botulinum toxin is proposed. Neurolytic agents may be preferred to botulinum toxin on a number of grounds, including earlier onset, potentially longer duration of effect, lower cost, and easier storage. Conversely, pain during injection, tissue destruction with chronic sensory side effects, and lack of selectivity on motor function with neurolytic agents may favor the use of botulinum toxin. Neurolytic agents and botulinum toxin may be used in combination, the former for larger proximal muscles and the latter for selective injection into distal muscles. In the future, neurolytic agents may prove more appropriate in very severely affected patients for whom the purposes of the block are comfort and hygiene. (ABSTRACT TRUNCATED)
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PMID:Traditional pharmacological treatments for spasticity. Part I: Local treatments. 982 83

High dose oral anti-spastic medication is effective in the treatment of spasticity but has the disadvantage of frequent systemic side effects such as drowsiness and general weakness. Therefore, neurolytic and chemodenervation procedures are further therapeutic options, especially in cases of local spasticity. Apart from phenol blocks with the risk of persisting painful dysesthesia, botulinum toxin type A (BtxA) appears to be a safe and effective treatment. In 204 patients (mean age, 41.5 years [range 3-91 years]) with acute (n = 29, mean duration of disease 2.9 months [range, 1-6 months]) and chronic (n = 175, mean duration of disease 111 months [range, 7-500 months]) spasticity due to stroke, traumatic brain and spinal injury and other lesions of the upper motor neuron, the effects of single-dose BtxA treatment were studied. An overall dose of 181.2 units [range, 15-600 units] of BtxA (Botox) was injected in a mean of 3.3 [1-14] muscles per patient. Results were assessed using a modified Rating of Response to BtxA (RRB, Brin et al. 1995). The RRB includes a pre- and post BtxA assessment of the severity of spasticity-associated problems (patient's self-assessment), a rating of the current percentage of normal function in the region of the body selected for BtxA and a global rating of changes induced by BtxA. 191 (93.6%) patients demonstrated improvement over a mean of 7.7 weeks [1-36]; no deterioration was observed. Mean overall severity and function improved significantly (p < 0.001). No systemic or severe side effects were registered. Only in 5.9% of the patients were mild (n = 10) or moderate (n = 2) reversible adverse events reported. We conclude that BtxA injections are safe and effective in the treatment of local spasticity.
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PMID:[Safety and tolerance of single-dose botulinum toxin Type A treatment in 204 patients with spasticity and localized associated symptoms. Austrian and German botulinum toxin A spasticity study group]. 1058 88

A 27-year-old woman was admitted to our hospital because of headache, fever and right neck pain. Neurological examination revealed mild meningeal signs, and hyper-reflexia in all extremities. In the laboratory tests, white-cell count was 13,000/mm3, rheumatoid factor(RF) and C-reactive protein(CRP) were positive. The cerebro-spinal fluid showed pleocytosis (56/mm3, neutorophils and lymphocytes were 26 and 28, respectively). Thus, she was diagnosed as aseptic meningitis. A few days later, she had weakness and dysesthesia of the right face and the left extremities. Pulse therapy with intravenous methylprednisolone was started. A magnetic resonance imaging (MRI) of the brain showed a hemorrhagic infarction in the right parietal lobe. In hemostatic markers, thrombin-antithrombin III complex(TAT; 106 ng/dl), D-dimer 1234 ng/dl, prothrombin fragment 1 + 2(F1 + 2; 2.36 nmol/L), beta-thromboglobulin (beta TG; 4,300 ng/dl) and platelet factor 4 (PF-4; 1,770 ng/dl) were extremely elevated. On duplex ultrasonography, a low echo lucent plaque was observed at the right internal carotid artery and the mean blood flow velocity in the right carotid artery was decreased. She was placed on oral prednisolone and warfarin for suspected stroke due to hypercoagulability associated with vasculitis. Afterwards, she discharged from our hospital. Two months later, she was readmitted to our hospital because of irregular menses and vaginal bleeding. Endometrial uterus biopsy was conducted, which revealed a grade I endometrioid adenocarcinoma. She was under total uterectomy without tumor recurrence. After the radical operation, white-cell count, RF, CRP, TAT, D-dimer, F1 + 2, and beta TG were normalized, and the mean flow velocity of the right common carotid artery was increased. Thereafter, she did not experience stroke recurrence. Therefore, we speculated that she had stroke due to hypercoagulability in association with malignancy, that is Trousseau's syndrome. We also assumed that aseptic meningitis, brainstem encephalitis associated with vasculitis in this patient are other clinical variants of paraneoplastic syndrome through immunological mechanisms associated with malignancy. We emphasize that patients with Trousseau's syndrome can be associated with other paraneoplastic manifestations such as vasculitis as seen in this patient.
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PMID:[A young patient with endometrioid adenocarcinoma who suffered Trousseau's syndrome associated with vasculitis]. 1247 93

The disinhibition hypothesis of post-stroke central pain (CPSP) suggests that 'the excessive response (dysesthesia/hyperalgesia/allodynia) is accompanied by a em leader loss of sensation' resulting from a lesion of a 'lateral nucleus' of thalamus or of 'cortico-thalamic paths' [Brain 34 (1911) 102]. One recent elaboration of this hypothesis proposes a submodality specific relationship, such that injury to a cool-signaling lateral thalamic pathway disinhibits a nociceptive medial thalamic pathway, thereby producing both burning, cold, ongoing pain and cold allodynia. The current study quantitatively evaluated the sensory loss and sensory abnormalities to discern submodality relationships between these sensory features of CPSP. The present results were statistically tested within individuals so that sensory loss and sensory abnormality are directly related by occurrence in the same individual. The results demonstrate that individuals with CPSP and normal tactile detection thresholds experience tactile allodynia significantly more often than those with tactile hypoesthesia. Most patients (11/13) exhibited hypoesthesia for the perception of cool stimuli, but few of these (2/11) showed cold allodynia. The most dramatic case of cold allodynia occurred in a patient who had a normal detection threshold for cold. Individuals with cold hypoesthesia, strictly contralateral to the cerebro-vascular accident (CVA or stroke), were often characterized by the presence of burning, cold, ongoing pain, and by the absence, not the presence, of cold allodynia. Overall, these results in CPSP suggest that tactile allodynia occurs in disturbances of thermal/pain pathways that spare the tactile-signaling pathways, and that cold hypoesthesia is neither necessary nor sufficient for cold allodynia.
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PMID:Allodynia in patients with post-stroke central pain (CPSP) studied by statistical quantitative sensory testing within individuals. 1515 97

A 30-year-old man was hospitalized with dysarthria and weakness of his right arm and leg. Three months previously, he had noticed numbness and weakness of his right shoulder, which spread to involve his left leg but which improved after 8 months. On admission, neurological examination revealed limb kinetic apraxia and constructive apraxia of the right hand, motor aphasia, dysarthria, and spastic quadriplegia. Sensory examination revealed hyperalgesia and dysesthesia in the right arm and left leg. Deep tendon reflexes were hyperactive in all four extremities. And he had bilateral Babinski signs. Laboratory examination revealed pH 7.38, PCO2 46.1 Torr, PO2 93.4 Torr, BE 1.7, and blood lactate, 9.0 mg/dl (normal 5-20 mg/dl). Cerebrospinal fluid lactate level was 20.0 mg/dl. pyruvate 1.34 mg/dl. and protein 83 mg/dl. Blood lactate and pyruvate values were markedly elevated after aerobic exercise. T2WI brain MRI showed scattered high signal lesions in the left precentral and postcentral gyrus, right paracentral lobes, both superior frontal gyri, and right superior temporal gyrus. Right biceps brachi biopsy showed almost complete cytochrome c oxidase (COX) deficiency. There were no ragged-red fibers. There was marked decrease of COX activity: 2.7 nmol/min/mg-mitochondrial protein (normal range: 33.0 +/- 16.1, n = 7) in the biopsied muscle. Open brain biopsy (after permission from the patient and his family) revealed gliosis and perivascular infiltration of lymphocytes and macrophages without vascular proliferation. There was no mitochondrial DNA mutations, deletion or duplication, including tRNA-Leu 3243, 8993, 3271, 9176, 3291, and tRNA-Lys 8344, 8356, and 8363. From these findings, a diagnosis of COX deficiency presenting as MELAS-like episodes was done. His mother also showed abnormality on aerobic exercise test, but she had no episode of stroke or neurological dysfunction. Six months later, his aphasia and apraxia of the right hand had resolved, and at discharge he was able to ambulate with a cane. Ten months later, he returned to his work. There has been no recurrence of neurologic symptoms over the next 3 years and 10 months. This patient appears to represent a rare case of adult onset COX deficiency presenting as MELAS-like episodes.
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PMID:[MELAS-like episodes in an adult case with cytochrome c oxidase deficiency]. 1523 72

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.
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PMID:[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]. 1551 11

The corticospinal motor evoked potential (MEP) evoked by motor cortex stimulation was investigated as an intraoperative index for the placement of stimulation electrodes in the epidural space over the motor cortex for the treatment of post-stroke pain. A grid of plate electrodes was placed in the epidural space to cover the motor cortex, sensory cortex, and premotor cortex employing a magnetic resonance imaging-guided neuronavigation system in two patients with severe post-stroke pain in the right extremities, a 66-year-old man with dysesthesia manifesting as burning and aching sensation, and a 67-year-old woman with dysesthesia manifesting as pricking sensation. The D-wave of the corticospinal MEP was recorded with a flexible wire electrode placed in the epidural space of the spinal cord during anodal monopolar stimulation of each plate electrode under general anesthesia. The grid electrode was fixed in position with dural sutures and the craniotomy closed. The effect of pain reduction induced by anodal monopolar stimulation of the same plate electrodes was examined using the visual analogue scale (VAS) on a separate day in the awake state without anesthesia. Comparison of the percentage VAS reduction and the recorded amplitude of the D-wave employing the same stimulation electrode revealed significant correlations in Case 1 (r = 0.828, p < 0.01) and Case 2 (r = 0.807, p < 0.01). The grid electrode was then replaced with two RESUME electrodes over the hand and foot areas, and the optimum positions were identified by D-wave recording before electrode fixation. Both patients reported satisfactory pain alleviation with lower stimulation voltages than usually required for patients with similar symptoms. These results indicate the potential of D-wave recording as an intraoperative indicator for the placement of stimulating electrodes over the motor cortex for pain relief.
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PMID:Recording of corticospinal evoked potential for optimum placement of motor cortex stimulation electrodes in the treatment of post-stroke pain. 1789 14


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