Biomedical subjects

N Peckham

Publications and source records attributed to N Peckham.

8 recordsLinked to original sources

PubMed1993

Electron microscopic changes in human pulps after intraligamental injection.

Because of its advantages, intraligamental injection is becoming a popular anesthetic technique to achieve anesthesia in vital pulps. This study investigated the possible effects of intraligamental injection on human pulps under electron microscope. Forty-two mandibular and maxillary premolars were scheduled to be extracted for orthodontic reasons after being anesthetized with intraligamental injections of 2% lidocaine, 1:100,000 epinephrine (experimental group). The same anesthetic solution was used on the contralateral teeth with either nerve or field blocks (control group). To examine the effects of ischemia on odontoblasts, 12 anesthetized premolars were extracted, and their pulps were placed in physiologic saline solution for different time intervals (15 minutes to 6 hours). The teeth in the experimental and control groups were then reanesthetized with nerve or field blocks of 3% carbocaine without epinephrine after time periods that ranged from 15 minutes to 28 days. After extraction, the teeth were sectioned vertically and their pulps were fixed in 3% glutaraldehyde. The odontoblastic layer of each pulp was examined under electronic microscope. Nuclear and cytoplasmic changes started an hour after ischemia in the pulps placed in physiologic saline. In contrast, little or no cellular changes occurred in pulps of the experimental or controls groups. On the basis of the results, it appears that intraligamental injection has no long-term deleterious effects on pulps of young human premolars.

Anesthesia, Dental↗

PubMed1991

The presence of nerve fibres in the coronal odontoblast layer of teeth at various stages of root development.

Many studies have investigated the presence of nerve fibres in the coronal odontoblast layer of mature teeth. However, little information is available on the presence of these structures in immature human teeth. The pulps of 18 human maxillary and mandibular third molars at various stages of development were collected, sectioned, and stained by the immunoperoxidase technique. The results showed the presence of numerous myelinated nerve fibres in the coronal odontoblast layer of teeth with fully formed roots. Similar observations were made in teeth with half formed roots, and in those without roots. On the basis of these results, it appears that a lack of response to vitality tests in teeth with incompletely formed roots is not wholly due to the absence of nerve fibres in the coronal odontoblast layer.

Dental Pulp↗

PubMed1987

Incontinentia pigmenti: association with anterior horn cell degeneration.

Incontinentia pigmenti (IP) has been associated with CNS involvement, including seizures, retardation, motor abnormalities, and malformations in greater than 30% of patients. Motor symptoms include spasticity and hyperreflexia; however, weakness and flaccidity have also been described. Peripheral nervous system neuropathology in patients with IP has not previously been reported. The infant with IP in this report showed generalized weakness due to anterior horn cell degeneration. The neuropathologic findings in both the central and peripheral nervous systems will be reviewed and contrasted to previous reports. Patients with IP and weakness should undergo neurodiagnostic evaluation of peripheral nervous system function.

Anterior Horn Cells↗

PubMed1987

Lumbosacral intramedullary myolipoma. Case report.

Intradural myolipoma is an unusual tumor. A case is described in which extramedullary and intramedullary striated muscle fibers caused gross contraction of a lipomatous tumor as well as of the spinal cord during electrical stimulation.

Humans↗

PubMedDate not supplied

Myoadenylate deaminase deficiency in children.

Myoadenylate deaminase (MADA) is an enzyme which participates in the purine nucleotide cycle necessary for energy production in human skeletal muscle. Approximately 35 patients with deficiency of this enzyme have been reported; one-half experienced their initial difficulties in childhood. Children with "primary" MADA deficiency typically have symptoms including muscle cramps, stiffness, and post-exercise myalgia and weakness. In "secondary" MADA deficiency, the clinical findings have been variable with delayed motor development, hypotonia, cardiomyopathy, delayed speech development, and generalized weakness. In most cases creatine kinase determinations, nerve conduction velocity studies, and routine muscle histopathology have been normal. Diagnosis has been established by demonstrating an absence of MADA activity by either direct muscle enzyme assay or histochemical staining. In this report we describe a 12-year-old boy with primary MADA deficiency and contrast his symptoms with those of previously described pediatric patients.

AMP Deaminase↗

PubMedDate not supplied

Infantile myositis: a case diagnosed in the neonatal period.

Infantile myositis is an inflammatory myopathy occurring in children under one year of age. This condition is extremely rare in the neonatal period and may be confused with other causes of generalized weakness. Creatine kinase activity is usually markedly elevated and electromyography demonstrates low amplitude, polyphasic motor unit activity. Muscle biopsy, necessary for diagnosis, documents characteristic findings of perifascicular atrophy and the presence of perivascular inflammatory cells. The diagnosis should be followed by corticosteroid treatment. The patient presented is the youngest biopsy-proved case of infantile myositis. In this report, his symptoms and clinical course are compared with those of previously described patients. The role of infectious agents and the immune state in the etiology of infantile myositis is considered.

Biopsy↗

PubMedDate not supplied

Anencephaly: clinical determination of brain death and neuropathologic studies.

Twelve liveborn anencephalic infants were serially examined to determine if they would meet our clinical criteria for whole brain death within a 7-day period: Protocol 1 infants (6) received intensive care including intubation from birth; and Protocol 2 infants (6) received intensive care during the period in which death was imminent. Brain death was determined by absence of brainstem function, including loss of all cranial nerve responses and sustained apnea (PCO2 greater than 60 torr) for 48 hours with confirmation of findings by an outside consulting child neurologist. The initial examinations of these 12 infants revealed spontaneous movements and startle myoclonus (12), suck, root, and gag responses (7), increased tone (8), deep tendon reflexes (9), absent pupillary responses (9), absent oculocephalic and corneal responses (6), absent auditory/Moro responses (7), and nonvisualization of the optic nerve (8). Mild depression of neurologic function occurred during the first several days of life; subsequently, the infants' responses were easier to elicit and more sustained. Only 2 infants met the clinical criteria for brain death. Neuropathologic findings indicated that observed complex motor responses were not based upon cortical activity because no infant had a normally-formed cerebrum. Brainstem neuronal activity may have accounted for these motor responses in some patients but even at this level neurons were scanty or absent. Our findings suggest that, although rare, clinical brain death can be determined in liveborn anencephalic infants; ophthalmologic and otologic developmental abnormalities may confound examination of cranial nerve function; and absence of cortical neurons supports the widely held opinion that these infants do not experience sensation.

Anencephaly↗

PubMedDate not supplied

The bright choroid plexus on MR: CT and pathologic correlation.

Fourteen patients studied with MR imaging were found, incidentally, to have unusually bright, large choroid plexus glomera on T2-weighted sequences. A group of 167 patients was then examined retrospectively for size and intensity of the choroid plexus glomera on T2-weighted images. In the latter group of 167 patients, 66 (39.5%) had bright choroid plexus glomera. Of those who had bright choroid plexus glomera, eight of the 14 initial group and 11 of the 66 patients studied retrospectively had previous CT scans. The typical CT appearance of these bright glomera consisted of nonenhancing central regions of low (but not negative) attenuation with peripheral calcifications in the majority. The remainder showed noncalcified glomera. Fifty-two glomera were obtained at autopsy and examined retrospectively. Eight showed small, variably sized masses with lipid deposits, neuroepithelial microcysts, and peripheral psammoma body calcifications. One patient who died had a bright choroid plexus glomus on MR, and his glomera showed the same pathologic findings. The autopsy findings were believed to be typical pathologically for early xanthogranulomata formation. These early xanthogranulomatous changes appear to be of little clinical significance but must be differentiated from other lesions that can produce bright or enlarged choroid plexus glomera on MR.

Adolescent↗