Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 221 children with head injuries and resultant deep coma followed for long-term problems, 156 became totally independent, functional individuals, only 61 lacking normal cognition and speech. Reconstructive surgical procedures for residual spasticity was necessary in 45 patients. Achilles lengthenings were the most common procedure performed; after Achilles lengthenings, toe flexor releases were most often required. Twenty children had anoxia from drowning or anesthesia problems; 7 of these had spastic hip deformities or dislocations, all within 6 months of the anoxic event. Progressive cerebrospastic syndromes and post-infectious cerebrospasticity most often require orthotic devices for their orthopedic management.
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PMID:Orthopedic management of acquired cerebrospasticity in childhood. 115 90

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

Previous reports on the incidence of heterotopic ossification (HO) in children and adolescents with traumatic brain injury (TBI) have ranged from 3% to 20%. These studies mention HO briefly or address patient cohorts with coma more than three months. We reviewed the medical records of 90 children younger than 19 years old, who were comatose more than 24 hours after TBI. Mean followup was 33.1 months (range = 2 to 128 months). Incidence of HO was 14.4% (n = 13). One to five sites were involved, with hip and knee most frequent, followed by shoulder, elbow, and nonjoint sites. Children with HO were older than 11 years (relative risk [RR] = 18.85, confidence interval [CI] = 3.7, 95.7), had a greater length of coma (RR = 7.22, CI = 1.4, 37.1), and had a greater associated risk for poor functional outcome (RR = 2.89, CI = 1.02, 7.9) compared to those without RO. Multiple limb fractures showed a trend toward association with increased incidence of HO. Other factors, including gender, history of skull fracture, brain CAT scan findings, and presence of spasticity, were not predictive of HO. Eleven children were treated with etidronate, four with nonsteroidal antiinflammatory drugs, and one with surgery. Only three children had residual functional impairments attributed to the presence of HO.
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PMID:Risk factors for heterotopic ossification in children and adolescents with severe traumatic brain injury. 158 Jul 74

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic profile of protirelin tartrate]. 212 84

Distinct chronic posttraumatic syndromes, ascribed to neurological deficits of patients suffering severe head injuries and being in prolonged coma, are much less frequently encountered in the literature than acute traumatic syndromes. The major components of the posttraumatic midbrain syndrome, resulting from compressive necrosis or vascular infarction at the midbrain level, are ipsilateral cerebellar signs (the predominant one being intention tremor), contralateral pyramidal signs (the predominant one being a spastic-dystonic hemiparesis), dysarthria, and mild to moderate intellectual impairment. Significant bilateral cerebellar dysfunction following head injury, without pyramidal, extrapyramidal, or pseudobulbar signs, constitutes a posttraumatic cerebellar syndrome. Its most disabling component, namely posttraumatic intention tremor, may be alleviated by thalamotomy. Following severe closed head injury, an infrequently encountered posttraumatic entity of dystonic hemiplegia or hemiparesis, which may be alleviated by thalamotomy, can occur, but does not have a specific neuroanatomical basis. Intention tremors following severe head injuries, rarely associated with hydrocephalus and without other significant cerebellar findings, can develop as a dysfunction of the cerebellofugal outflow system. While chronic posttraumatic syndromes can be complex and difficult to treat, cerebellar stimulation has been utilized ipsilaterally to modulate limb spasticity, and bilateral ventrolateral cryothalamectomies staged 4-6 months apart have been successful in alleviating severe (intractable) intention tremors.
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PMID:Rehabilitative neurosurgery: posttraumatic syndromes. 262 1

Inverse ocular bobbing (IOB) is an uncommon abnormal eye movement. Its characteristics are slow downward eye movement with rapid upward return, a nadir at the extreme of downgaze position and horizontal roving eye movement. We present a case of IOB associated with cerebral embolism and diabetes insipidus. A 69 year-old right-handed woman was admitted because of a consciousness disturbance. She had been well until November 10, 1983, when she was found dysarthric and left hemiplegic. On admission, she was stuporous. There were conjugate deviation to the right, central left facial and hypoglossal palsy, left hemiplegia with spasticity, left hyperreflexia with positive pathologic reflex and anosognosia. A CT scan performed on November 11 showed extensive hypodense area in the region supplied by the right middle cerebral artery. A right carotid angiography revealed multiple occlusions in the top of the right internal carotid artery with poor collateral circulation. After admission, the level of consciousness gradually deteriorated and became comatose on November 18, when the following abnormal eye movements were observed. Following spontaneous horizontal roving eye movement, both eyes deviated downward slowly from midposition, taking 1 to 2 seconds to reach the nadir. The eyes then remained in the position for 1 to 15 seconds, followed by a rapid return to the midposition. These abnormal eye movements are compatible with inverse ocular bobbing (IOB) described by Knobler. Electronystagmography detected typical IOB and spontaneous upward nystagmus. There was no evidence of hypoxia when these abnormal eye movements were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inverse ocular bobbing associated with cerebral embolism and diabetes insipidus--a case report]. 274 84

The expanding use of intrathecal baclofen for spasticity has raised a concern about the treatment of overdose in these patients, since no specific baclofen antagonist is available. Since physostigmine has been reported to reverse the respiratory depression and somnolence due to opiates, the drug was tried for the treatment of baclofen overdose. In three cases, intravenous physostigmine (2 mg) completely reversed the respiratory depression and coma caused by boluses of 80 to 800 micrograms of lumbar intrathecal baclofen. Physostigmine, although not a specific antagonist, should provide increased safety for patients receiving intrathecal baclofen.
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PMID:Physostigmine in the treatment of intrathecal baclofen overdose. Report of three cases. 274 50

The influence of memantine on several properties of a neuronal cell line was tested. The aim was to get some insight into possible mechanisms of action of this drug which is therapeutically applicable in treatment of spasticity, Parkinson's disease, and cerebral coma. In neuroblastoma X glioma hybrid cells, memantine, at micromolar concentrations, blocked the depolarization induced by iontophoretically applied serotonin (5-hydroxytryptamine, 5-HT). In the hybrid cells, receptors of the 5-HT3 type mediated the depolarization, which was frequently accompanied by a series of action potentials. The inhibition by memantine of the serotonin response occurred fast and was completely reversible, irrespective of whether the cell showed a stable membrane potential or spontaneous action potentials. However, memantine did not alter spontaneous or electrically evoked action potential activity in the hybrid cells, and apparently did not block the underlying ionic conductances. Furthermore memantine did not affect either the cation permeability activated by substance P in the hybrid cells or the K+ channel triggered by bradykinin in a glioma cell line. Thus, memantine appears specifically to suppress the ion channel opened by serotonin in the hybrid cells. The interaction of memantine with serotonin receptors and the associated ion channels reported here, might give an important clue, as to a site of action of memantine in the nervous system.
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PMID:Memantine (1-amino-3,5-dimethyladamantane) blocks the serotonin-induced depolarization response in a neuronal cell line. 335 74

Septo-optic dysplasia (De Morsier's syndrome) is a common cause of congenital optic nerve hypoplasia. Associated abnormalities such as hypothalamic/pituitary dysfunction, hypotonia or spasticity, may result in affected children presenting for surgical procedures under general anaesthesia. A 3.5-year-old boy with the undiagnosed condition had his Achilles tendons elongated under an uncomplicated general anaesthetic. The postoperative period was complicated by coma and a major convulsive seizure which responded to glucose and steroids. The importance of awareness of this condition in short children with poor visual acuity who require general anaesthesia is stressed, and the presenting features of seven other cases are demonstrated.
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PMID:Anaesthesia and septo-optic dysplasia. Implications of missed diagnosis in the peri-operative period. 343 62

A 4-year-old Black child was admitted to hospital in coma and with retinal hemorrhages. He was diagnosed as having Reye's Syndrome and remained hospitalized for 1 month. At discharge, he was neurologically compromised with spasticity of the right arm and leg, and could not walk or sit unsupported. Three weeks later he was again seen in the emergency room with a swollen right arm and leg and was subsequently readmitted. Healing fracture of the right femur and probable healing fracture of the right humerus were diagnosed. These were thought to be due to a fall from a stroller. Almost 4 months later, the child died at his home in the care of his mother's boyfriend. Autopsy findings were consistent with a severely chronically battered child.
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PMID:Battered child syndrome in a four year old with previous diagnosis of Reye's syndrome. 395 91


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