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Biomedical subjects

O Papazian

Publications and source records attributed to O Papazian.

At least 19 recordsLinked to original sources

Neoplasm as a cause of brachial plexus palsy in neonates.

Two patients with neonatal onset of arm weakness resulting from neoplastic involvement of the brachial plexus who were initially considered to have obstetric brachial plexus palsies are reported. The first patient was a 7-day-old female who presented with a left supraclavicular mass that was first detected at 2 days of age and left proximal arm weakness. The weakness involved the whole arm within 3 days. The mass was a malignant rhabdoid tumor. The second patient was a 28-month-old male who presented with slowly progressive right arm weakness, which began at 3 weeks of age, and episodes of scratch marks on the arm that began at 4 months of age. Magnetic resonance imaging revealed a plexiform neurofibroma of the brachial plexus. The features that are suggestive of a brachial plexus palsy caused by a neoplasm rather than of obstetric brachial plexus palsy include the following: the onset of weakness after the first day of age, with a progressive course; a history of a normal delivery and birth weight; the absence of signs of a traumatic injury or injuries; the appearance before 7 days of age of a growing supraclavicular mass without radiographic evidence of a clavicular fracture; and recurrent scratch marks on the weak arm.

Arm↗

Focal upper extremity neuropathy in neonates.

Focal upper extremity neuropathies are common in neonates. The brachial plexus is the most common site involved. Brachial plexus injuries may involve different structures, thus producing different clinical presentations: complete brachial plexus palsy, Duchenne-Erb palsy, upper-middle trunk brachial plexus palsy, Klumpke palsy, fascicular brachial plexus palsy, and bilateral brachial plexus palsy. The causes of brachial plexus palsy are obstetric injury, intrauterine compression, humeral osteomyelitis, hemangioma, exostosis of the first rib, neck compression, and neoplasm. The differential diagnosis of brachial plexus palsy includes pseudoparesis, amyoplasia congenita, congenita varicella syndrome, and neurological lesions at other neuroanatomical levels. The cause and the degree of injury dictate the prognosis. The prognosis of obstetric brachial plexus injury is usually good.

Arm Injuries↗

Neurophysiological evaluation of children with traumatic radiculopathy, plexopathy, and peripheral neuropathy.

Neurophysiological evaluation of children with traumatic peripheral nervous system injury is accomplished with electromyography, motor and sensory nerve conduction studies, and somatosensory and motor-evoked potentials. Preoperative neurophysiological tests are performed if motor deficits persist for more than 3 months. Evidence of reinnervation on these neurophysiological tests predates clinical recovery by weeks, hence they help determine the site of the lesion and provide objective measures for selecting candidates for surgical exploration. Intraoperative neurophysiological tests help to identify and confirm the integrity of nerves and to develop the optimal surgical strategy. Postoperative evaluations every 3 to 6 months may determine efficacy of treatment.

Brachial Plexus Neuropathies↗

Single photon emission computed tomographic evaluation of brainstem release phenomenon and seizure in neonates.

We report the ictal brain single photon emission computed tomographic (SPECT) findings in two neonates. One neonate had hypoxic-ischemic encephalopathy, a disorganized discontinuous electroencephalogram (EEG) background, lethargy, seizures, and brainstem release phenomena. A brain SPECT was performed during a brainstem release phenomenon characterized by a 34-second sustained tonic posture of the right arm and chewing. It did not reveal focal cerebral hemisphere hyperfusion. The second neonate had hemimegalencephaly, low-voltage irregular EEG background, and seizures. A brain SPECT was performed during a seizure characterized by a 32-second sustained tonic posture of the right arm. It revealed focal hyperperfusion in the posterior region of the left hemisphere. The brain SPECT findings in these patients indicate that despite clinically similar events, brainstem release phenomena and seizures have different perfusion characteristics, and refute the theory that brainstem release phenomena are due to epileptic foci in the cerebral hemispheres undetectable by EEG.

Brain↗

Intravenous valproate dosing in neonates.

The loading dosage of intravenous valproate required to achieve a desired serum concentration in neonates is not known. Two neonates with seizures received loading doses of intravenous valproate over 30 minutes. Serum valproate concentrations were measured 45 minutes and 3 hours after initiation of the infusion. Both neonates had received phenobarbital and phenytoin before the loading infusions. In the first patient, a loading dose of intravenous valproate of 10 mg/kg increased the 45-minute postinfusion serum valproate concentration to 41 microg/mL with a 3-hour postinfusion serum valproate concentration of 33 microg/mL. In the second patient, a loading dose of 25 mg/kg increased the 45-minute postinfusion serum valproic acid concentration to 100 microg/mL with a 3-hour postinfusion serum valproic acid concentration of 78 microg/mL. We found that each 1 mg/kg of intravenous valproate increased the 45-minute and 3-hour postinfusion serum valproic acid concentrations by approximately 4 microg/mL and 3 microg/mL, respectively. We suggest that these figures be used to calculate the desirable loading dose of intravenous valproate in neonates until larger studies are conducted. The volume of distribution and the serum clearance of valproate were approximately 0.245 L/kg and 25 mL/h/kg, respectively.

Anticonvulsants↗

Similar brain SPECT findings in subclinical and clinical seizures in two neonates with hemimegalencephaly.

Brain single-photon emission computed tomography (SPECT) findings during clinical and subclinical seizures were compared in two neonates with hemimegalencephaly. Interictal and ictal brain SPECT were performed in two neonates. The ictal studies were performed during a clinical seizure in one neonate and during a subclinical seizure in another neonate. They revealed similar focal hemispheric hyperperfusion at the electroencephalographic seizure foci in both cases. The similar perfusion patterns imply that clinical and subclinical seizures place similar metabolic demands on the cerebral tissue involved in the generation of electroencephalographic seizures in neonates with cerebral dysgenesis and suggest that clinical and subclinical seizures should be treated similarly in this population.

Brain↗

[Clinical presentations, differential diagnosis and management of obstetric brachial palsy].

INTRODUCTION: The brachial plexus originates from C5 to T1 spinal segments. The brachial plexus includes the ventral ramus, trunks, divisions, cords and branches. DEVELOPMENT AND CONCLUSIONS: Brachial plexus injuries produce clinical syndromes. The Duchenne-Erb syndrome is the most frequent presentation of obstetric brachial plexus injury. The differential diagnosis of brachial plexus palsy include decreased arm movements due to pain, or weakness caused by a lesion of the nervous system outside in the brachial plexus, or by a lesion in the brachial plexus due to non-obstetrical causes. Management of these patients initially includes considering the possibility of clavicular and humeral fractures and posterior subluxation of the shoulder; and subsequently considering the possibilities of subscapularis muscle contraction or posterior shoulder subluxation in patients that develop internal rotation contracture of the shoulder; or flexion, pronation or supination contracture in patients with forearm deformation. Treatment consist of physical therapy, administration of botulinum toxin, electrical stimulation, neurolysis, nervatization, removal of neuromas and nerve grafting, treatment of fractures and subluxation, release of muscle contracture and tendon transplantation.

Brachial Plexus↗

[Neurophysiological assessment of children with obstetric brachial plexus palsy].

INTRODUCTION: The objectives of the neurophysiological evaluation of infants with brachial plexus palsy are to determine the time of occurrence of the lesion, to locate the lesion and to determine its course. METHODS AND CONCLUSIONS: These objectives are achieved by studying affected upper extremity muscles by needle electromiography (EMG) and affected nerves by motor and sensory conduction studies. EMG is performed in the first week of life in those patients with brachial plexus palsy of unknown etiology to determine the age of the lesion for medico-legal reasons. EMG is performed before surgery for tendon transfer in the selected muscles to assure that they are normal. EMG and motor and sensory conduction studies are performed at the age of 3 and 6 months in infants with less than 4 muscle weakness to determine candidates for surgical exploration. Motor and sensory nerve conduction studies are performed intraoperative to determine the functional status of the affected axons and the best surgical procedure (neurotization, neurolysis and/or neuroma resection and homologous nerve graft).

Brachial Plexus↗

[Surgical treatment of children with brachial plexus paralysis].

OBJECTIVE AND METHODS: A variety of surgical procedures exist for early repair of the nerve injury in obstetrical brachial plexus palsy, including neuroma excision and nerve grafting, neurolysis and neurotization. Secondary deformities of the shoulder, forearm, and hand can similarly be reconstructed using soft tissue and skeletal procedures. This review describes our surgical approach to maximize the ultimate functional outcome in infants and children with obstetrical brachial plexus palsy.

Brachial Plexus↗

[Epilepsy centers: classification and basic requirements].

Over the last two decades the surgical treatment of epilepsies has become a commonly used and effective method for the treatment of intractable epilepsy. However, because of its wide use in various types of centers throughout the world the methodology involved varies significantly throughout the centers. With this article we propose the bases from which a multidisciplinary team of numerous centers can eventually develop an effective and acceptable international protocol for the surgical treatment of the epilepsies and the classifications of the centers.

Epilepsy↗

Bilateral tonic-clonic epileptic seizures in non-benign familial neonatal convulsions.

We report an electroclinical pattern considered characteristic of benign familial neonatal convulsions (BFNC) in two neonates without BFNC. Both neonates were products of uncomplicated pregnancies, labor, and deliveries. The cause of the seizures was not established. There was no family history of seizures or epilepsy. Seizures started on the second and third days after birth. Ten seizures were captured by continuous video-EEG telemetry. The electroclinical events began with generalized tonic posturing coinciding with the appearance of diffuse attenuation of the EEG activity. After several seconds, bilateral clonic movements accompanied by bilateral repetitive sharp waves or spikes occurred in the EEG. One patient had normal development; the other became autistic. We conclude that the electroclinical pattern occurring in BFNC can occur in other types of neonatal seizures.

Autistic Disorder↗

[The evaluation of a newborn in a coma].

Coma is differentiated from sleep by the absence of a normal arousal response and from death by the presence of heart beats and the absence of brain death criteria. Most causes of coma are readily diagnosed and treated. Others require a test whose results are not immediately available, transportation or a risky procedure and empirical treatment has to be considered. In addition to treating the cause of coma, treatment of the systemic and neurological causes of secondary brain damage is paramount.

Cerebral Hemorrhage↗

[Cerebral palsy therapy].

Unfortunately, in spite of the advances in foetal and perinatal medicine in the last twenty years, the incidence of cerebral palsy has remained unchanged (1.5-2.5 per 1000 live births). It has even possibly risen slightly in premature babies of low birth weight, in parallel with the increased survival of these babies. In spite of modern techniques of rehabilitation, 25% of these patients cannot walk and 35% are mentally retarded. This costs society 5,000 million dollars annually, not counting the loss of opportunity and the emotional and economic burden imposed on these families. The development of new preventive measures such as the use of antagonists of the cortical excitatory amino acids (which when in excess may cause irreversible cerebral damage in cases of hypoxic-ischaemic encephalopathy of the new born). Intramuscular botulinum toxin and continuous intrathecal baclofen seem to promise a reduction in the incidence and functional incapacity of cerebral palsy.

Anti-Dyskinesia Agents↗

[Single photon emission computer tomography in the differential diagnosis of the paroxysmal clinical events in newborns].

Conventional computerized cranial tomography by single photon emission (TLCESF) is a nuclear medicine technique which makes use of a radioactive chemical complex to obtain a qualitative image of cerebral, cerebellar and brain-stem vascularization. This technique shows the changes in vascularization which occur between (decrease) and during (increase) the clinical events of paroxysmal epilepsy (ECP) in the area of origin. This technique is indicated in neonates with ECP which does not disappear on etiological treatment, where a non-epileptic cause cannot be ruled out on clinical grounds and where there are no associated encephalographic epileptic changes during the ECP.

Brain↗

Reversible dementia and apparent brain atrophy during valproate therapy.

Two children developed severe cognitive and behavioral deterioration suggestive of a degenerative disease while being treated with sodium valproate for idiopathic, localization-related epilepsy with centrotemporal spikes. Magnetic resonance imaging revealed marked central and generalized cortical and cerebellar atrophy. In both patients, clinical symptoms and signs cleared in a few weeks following valproate withdrawal. The magnetic resonance imaging appearance improved within 3 months in 1 of the patients and normalized in both after 6 and 12 months. No metabolic changes were associated with the clinical or imaging abnormalities. Although the mechanism of this rare idiosyncratic complication of valproate therapy is unknown, we advocate discontinuing valproate therapy in all epileptic patients with neuromental deterioration or brain atrophy of unknown etiology.

Atrophy↗

Cuban embargo.

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Commerce↗