Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spinal cord seizures are infrequently reported. They have been associated with intravenous dye placement, transverse myelitis and multiple sclerosis, but never with traumatic spinal cord injury (SCI). We report the case of a 48-year-old SCI male with complete C6 quadriplegia, and apparent spinal cord seizures. These seizures were characterised by myoclonus simplex activity involving the upper extremities only. The lower extremities were spared. The patient was conscious throughout the myoclonic activity and an electroencephalogram of the brain obtained during an event revealed no cortical epiliptiform activity. The seizures lasted approximately 30 seconds to a few minutes, and an acute increase in blood pressure and a decrease in pulse generally occurred 30 to 60 seconds prior to the event. Previously reported spinal cord seizures in multiple sclerosis were frequently treated with carbamazepine. In this case successful treatment was with diazepam. Spinal cord seizures may present in those with traumatic SCI. Benzodiazepines may be useful in the treatment of spinal cord seizures.
Paraplegia 1991 Oct
PMID:Spinal cord seizures: a possible cause of isolated myoclonic activity in traumatic spinal cord injury: case report. 177 64

We report a patient who developed paraplegia following percutaneous nephrolithotresis of the left kidney under epidural anaesthesia. The cause of the paraplegia was unknown, but occlusion of the anterior spinal artery or central arteries and arachnoiditis, possibly due to the epidural anaesthesia, may have taken part in the onset and progression of the paralysis. The patient had spinal myoclonus corresponding to the spinal levels where myelomalacia was found by magnetic resonance (MR) imaging.
Paraplegia 1991 Feb
PMID:Post-operative paraplegia with spinal myoclonus possibly caused by epidural anaesthesia: case report. 202 78

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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PMID:The AIDS dementia complex: I. Clinical features. 372 8

We describe a patient with a longstanding paraplegia who developed spinal myoclonus on 3 different occasions spanning one year, once after an enhanced CT scan and twice after excretory urographies, one of which was also followed by a generalized tonic-clonic seizure. To our knowledge only one case of spinal myoclonus secondary to the administration of intravenous contrast material in a patient with a spinal arteriovenous malformation has yet been reported. Taken together, the findings in these cases suggest that spinal myoclonus following intravenous iodine administration is indicative of an underlying spinal cord lesion.
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PMID:[Spinal myoclonus secondary to the intravenous administration of iodine contrast media]. 747 10

Four cases of spinal myoclonus are described, three males and one female. The mean age was 51 years (28-75 years). The mean time between the onset of the myelopathy and the myoclonic jerks was 4.3 months (1-8 months). The involuntary movements were determined by trauma, Devic's disease, tuberculous myelopathy and tumor. Three patients had spastic paraplegia with bilateral myoclonus more evident on the right side. The fourth patient had a flaccid paraplegia with symmetrical jerks. The data suggest that different processes (trauma, demyelinating, infection and tumor) affecting the spinal cord may cause the same type of involuntary movements.
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PMID:Spinal myoclonus: report of four cases. 814 51

Propriospinal myoclonus is a rare and relatively little studied complication of spinal cord injury. We report two patients with an extension-producing myoclonus presenting with tetraplegia caused by cervical trauma. Rhythmic extension jerks of the trunk and lower limbs appeared several weeks after their injury in a context of severe spasticity. The characteristics of these jerks were determined by polymyography of 12 muscles. They lasted between 306 and 1127 ms with a frequency of 0.3 to 0.5 Hz. By comparing latencies their origin was found to be in the lumbar cord from which there was a slow (2 m s-1) upward and downward spread. Oral treatment with baclofen and sodium valproate was partially successful in one patient, but ineffective in the other. Intrathecal 75 or 100 micrograms baclofen produced a striking, complete disappearance of myoclonus prompting the implantation and successful use of a baclofen pump in one patient. These two new cases suggest the existence of a lumbar generator in which myoclonic extension jerks originate, and demonstrate a new therapeutic alternative in intrathecal baclofen for patients resistant to oral medication.
Paraplegia 1995 Nov
PMID:Propriospinal myoclonus in tetraplegic patients: clinical, electrophysiological and therapeutic aspects. 858 5

Biermer disease or pernicious anemia is an autoimmune atrophic gastritis characterized by the lack of secretion of gastric intrinsic factor. This leads to an insufficient absorption of vitamin B12 in the ileum. Clinical manifestations are mainly hematologic. Neuropsychiatric manifestations are known but are less frequent especially early in the disease. Inaugural neuropsychiatric arrays are rare and various thus making diagnosis difficult. In this article, we report through two clinical cases different neuropsychiatric manifestations revealing pernicious anemia. Mrs. C.O., aged 56, presented after surgery for gallstones, an acute psychiatric array associated with gait disorders. She had no history of neurological or psychiatric problems. The psychiatric interview revealed delirious syndrome, depressive symptoms and anxiety. Neurological examination noted a flaccid paraplegia with peripheral neuropathic syndrome and myoclonus in the upper limbs. At the full blood count, a macrocytosis (VGM: 112.2fl) without anemia was found. The level of vitamin B12 in the blood was low. Cerebro-spinal MRI was suggestive of a neuro-Biermer and showed hyper signal in the cervical cord on T2-weighted sagittal section. In axial section, hyper signal appears at the posterior columns in the form of V. There were no brain abnormalities. A sensorimotor axonal polyneuropathy was diagnosed. The patient received vitamin B12 intramuscularly for ten days associated with neuroleptic treatment. Mrs. R.M., aged 40, was brought to the psychiatry consultation for acute behavioral disorders progressively worsening over a month. An anxiety syndrome, depressive syndrome and delirious syndrome were identified. Neurological examination showed a posterior cordonal syndrome with quadripyramidal syndrome. Full blood count showed a macrocytic anemia. Serum B12 level was collapsed. Cerebro-spinal MRI was normal. She received vitamin B12 with clinical and biological improvement. Features of pernicious anemia vary according to studies and age range. Digestive and hematological manifestations are well known. Neurological and psychiatric manifestations of pernicious anemia were also described in the early literature. They can be the initial symptoms or the only ones. However, inaugural neuropsychiatric features are often unrecognized. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. Neurological involvement includes mainly combined spinal sclerosis, peripheral neuropathy and dementia. Cerebellar ataxia and movement disorders are reported less often. Severity of neuropsychiatric features and therapeutic efficacy depends on the duration of signs and level of B12 deficiency. Macrocytic anemia may lack. Neuropsychiatric manifestations could be isolated or be the first manifestation of vitamin deficiency and occur without any hematological or gastrointestinal context. Pernicious anemia and serum B12 assay should be discussed in all patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. Nevertheless, B12 level could be normal in genuine pernicious anemia diseases and macrocytic anemia may lack. Substitutive vitaminotherapy is required when diagnosis is strongly suspected and etiologic assessment is negative.
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PMID:[Neuropsychiatric manifestations ushering pernicious anemia]. 2634 54