Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The disorders of ocular motility seen in association with brainstem or cerebellar disorders may point to rather specific anatomical or pathological correlations. Pontine gaze palsy reflects involvement of the pontine paramedian reticular formation. Internuclear ophthalmoplegia signifies a lesion in the medial longitudinal fasciculus. Skew deviation may result from a lesion anywhere in the posterior fossa. Ocular bobbing typically results from a pontine lesion. The Sylvian aqueduct syndrome is characteristic of involvement in the upper midbrain-pretectal region, usually a pinealoma. Cerebellar lesions may be manifested by gaze paresis, skew deviation, disturbances of saccadic or smooth pursuit movements, ocular myoclonus, or several characteristic forms of nystagmus. Familiarity with these disorders may be of great help to the physician dealing with a patient with a possible posterior fossa lesion.
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PMID:Abnormal ocular motility with brainstem and cerebellar disorders. 34 6

A patent, who suffered from nonprogressive athetotic-myoclonic hyperkinesia of the left arm and spastic paresis of the underdeveloped left leg since early childhood, experienced a febrile episode at the age of 23, after which a weakness and ataxia of the right limbs with frequent falling persisted; at the age of 28, he developed a right-sided rigidity, tremor at rest and mask-like face as sequelae of encephalitis disseminata exacerbations. The violent intention myoclonus of the left side of the body could be abolished by stereotactic coagulation in the V.o.p and V.o.a and zona incerta until death 11 days later. The athetotic myoclonic hyperkinesia is the consequence of a left-sided severe status marmoratus of the right putamen with extensive loss of nerve cells and shrinkage. The additional nerve cell loss in the right substantia nigra due to demyelinating encephalitic foci did not produce Parkinson symptoms, because these require a normal striatum. This loss did, however, exaggerate the original hyperkinesia to a violent intention myoclonus, which was abolished by interruption of denatatothalamic afferents to the V.o.p nucleus and of pallidothalamic afferents to the V.o.a nucleus. The Parkinson syndrome of the right side is due to demyelinating foci of different ages. The Parkinson symptoms were manifest on the right side, because the left status marmoratus did not severely reduce the striatal nerve cells. In this case, there is no indication that the introduction of the stereotactic electrode has precipitated new demyelinating foci.
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PMID:Stereotactic treatment of action myoclonus in a case of combined status marmoratus and multiple sclerosis. A contribution to the pathophysiology of basal ganglia with multiple lesions in both the striatum and the substantia nigra. 109 75

Immediately after a patient with myoclonus epilepsy smoked a nicotine-containing cigarette, tetraparesis and hyperreflexia with ankle clonus developed, but disappeared within several minutes. During paresis, the H-reflex size of the soleus muscle increased, EEG showed more slow waves than before smoking, and the cerebral perfusion increased around the motor cortex as shown by single photon emission CT. A similar effect occurred when the patient chewed nicotine gum, and smoking a cigarette with a high nicotine content induced severe positive and negative myoclonus after the development of tetraparesis. Administration of the C6-type nicotinic antagonist mecamylamine not only countered the smoking effect, but ameliorated the spontaneous positive and negative myoclonus. Mecamylamine may prove useful for the treatment of positive and negative myoclonus in myoclonus epilepsy.
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PMID:Nicotine-sensitive paresis. 173 70

Ten patients with involuntary leg movements due to myelopathy were studied clinically and polysomnographically. The clinical manifestation and polysomnographical findings of involuntary leg movements were identical to sleep-related periodic leg movement (PLM) (nocturnal myoclonus). Since 2 patients had complete transection of spinal cord due to injury or vascular accident, the spinal cord deprived of supraspinal influences was considered to generate the rhythm of PLM. Suppression of the leg movements during REM sleep was not obvious in the patients with complete transection of spinal cord. In addition, PLM alternated from one side to the other 1-4 times a night with intervals of 1-4 h in all patients. This alternation also seemed to be from the spinal cord. This PLM of spinal cord origin was different from spinal myoclonus in their clinical features although both were generated within the spinal cord. PLM of spinal cord origin showed a triple flexion of the ankle, knee and hip, and this was very similar to a flexor withdrawal reflex which all patients exhibited. Therefore, it was suggested that PLM of spinal cord origin has a common mechanisms with spinal automatism. Although all patients had extensor plantar responses, PLM preceded the paresis in three patients and the severity of paresis was variable. There was no laterality of left and right PLMs even in patients with weakness of the leg on one side. This suggested that PLM of spinal cord origin might be induced by the interruption of the tract which was separate from, but runs near the corticospinal tract.
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PMID:Sleep-related periodic leg movements (nocturnal myoclonus) due to spinal cord lesion. 191 96

Any attempt to classify and to understand the basic mechanism underlying the neurological symptoms as pyramidal and/or sensitive, should start from the fundamental laws of nervous system functioning: 1) the law of reciprocal innervation of Sherrington; 2) the law of hierarchy of levels of Jackson and 3) the law of supersensitivity of deafferented structures of Cannon. Paresis on one side, Jacksonian jerks on the other side represent two opposite conditions known respectively as negative and positive symptoms of corticomotor involvement. Unluckly involuntary movements cannot be explained with these three laws. They are the clinical expression of the disorganization and disintegration of functions: a true disregulation unrespectful of laws and general principles. They must be considered as the result of conflicts of antagonist functions controlling each other, i.e. tremor, chorea, myoclonus, torsion spasm etc. The author emphasizes the clinical-descriptive aspect of the problem.
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PMID:[Involuntary movements]. 269

Chronic, relapsing myelitis has been induced in golden Syrian hamsters by the intracerebral inoculation of measles virus when the animals were less than 1 day old. No acute illness was seen in animals that developed myelitis, and the onset of the myelitis was at 5 to 50 weeks after infection. In most animals the illness was slowly progressive, with hindquarter myoclonus being the most common clinical sign. Occasionally the disease involved episodic limb paresis with nearly total recovery of limb function between periods of paralysis. In most animals pathologic changes were confined to the spinal cord and involved mononuclear cell infiltration, marked gliosis, widespread demyelination, and necrosis. Virus could not be isolated from nervous tissue by cocultivation techniques, and virus-specific immunofluorescence could not be detected. The strain of virus used was distinctive in that it contained high levels of a naturally occurring viral variant that differs from typical measles virus in several distinctive ways.
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PMID:Chronic, relapsing myelitis in hamsters associated with experimental measles virus infection. 693 80

Cell-free viruses recovered from virus-carrying cultures of the Niigata-1, Kitaken-1, and Biken strains of SSPE virus were examined for neurovirulence. The cell-free viruses were prepared by freezing and thawing or by EDTA treatment of the virus-carrying cultures and inoculated into adult mice intracerebrally. A considerable number of the inoculated mice showed clinical signs about 1 to 5 weeks after the inoculation. The first symptom was hyperreactivity, which was followed by paresis and myoclonus. All of the affected mice fell in paralysis and finally died. The virus could be recovered from the moribund mice by cocultivation of the brain cells with Vero cells. Immunofluorescence staining of the brain tissue revealed that infected cells containing viral antigens were distributed sparsely. No inflammatory feature, however, was observed in the brain as far as examined and neutralizing antibody against SSPE virus was not detected in sera from the mice inoculated with the cell-free SSPE viruses.
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PMID:Mode of subacute sclerosing panencephalitis (SSPE) virus infection in tissue culture cells. III. Neurovirulence of cell-free SSPE viruses of Niigata-1, Kitaken-1, and Biken strains. 731 88

The neurophysiological findings in eight patients with the stiff man syndrome (SMS), including four of six tested with autoantibodies against glutamic acid decarboxylase, are presented. Neurophysiological findings did not make it possible to discriminate between patients with and those without autoimmunity against GABAergic neurons. Investigation of mono- and polysynaptic reflexes revealed abnormal results in a variable number of SMS patients, the abnormalities largely corresponding to those seen in spastic paresis. A stereotyped motor response to electrical stimulation of peripheral nerves was recorded from the trunk muscles of all patients investigated. This response was termed spasmodic reflex myoclonus and consisted of a sequence of 1-3 synchronous myoclonic bursts, 60-70 ms after median nerve stimulation, followed by a tonic decrescendo activity over a number of seconds. The recruitment order of muscles along the neuraxis in spasmodic reflex myoclonus suggested that the latter was generated in the spinal cord and conveyed via propriospinal tracts. It is thought that spasmodic reflex myoclonus may serve not only as a diagnostic tool, but also as a key to understanding some aspects of the pathophysiology of both spasms and stiffness in SMS. It is speculated that stiffness is a fragment of spasms, both being generated by common neuronal mechanisms tentatively ascribed to interneurons in the spinal grey matter.
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PMID:Stiff man syndrome: neurophysiological findings in eight patients. 883 47

A 48-year-old female developed apraxia, followed by aphasia and dementia. Clinical examination also showed an alien member sign, supranuclear gaze paresis, myoclonus and rigidity on the right arm. The examination of the frontal lobe biopsy showed typical lesions of Alzheimer's disease as the only neuropathological abnormality. The association of this clinical syndrome with Alzheimer's pathology is unusual.
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PMID:[Alien limb behavior associated with Alzheimer's disease]. 780 54

At least three types of ictal atomic phenomena can be seen in partial seizures. Focal atomic seizures are partial seizures with ictal paresis or paralysis of one or more body parts preceding or independent of any convulsive activity. A diagnosis may be difficult without simultaneous EEG recording supplemented by video monitoring or polygraphy. Epileptic negative myoclonus manifests as brief lapses in tone in one or more muscle groups that interferes with motor coordination and postural control. Drop attacks can also occur in partial seizures, as have been well documented in patients with temporal or frontal lobe epilepsy. Different mechanisms may underlie these three phenomena. Focal atonic seizures probably result from relatively circumscribed seizure activity in one or more cortical areas that contribute to the elaboration and execution of motor functions. Whether this represents inactivation or interference in motor integration, or activation of inhibitory system, remains unresolved. The pathophysiology of epileptic negative myoclonus, like that of its positive counterpart, is probably to be found at a more local level, possibly from transiently enhanced local inhibition in the motor cortex. Drop attacks in partial seizures may be close in mechanism to that also seen in generalized seizures, possibly related to ictal activation of descending inhibitory pathways in the brainstem.
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PMID:Atonic phenomena and partial seizures. A reappraisal. 884 76


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