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PubMed1987

Optic nerve dysfunction in familial dysautonomia.

We examined 12 patients with familial dysautonomia who had clear corneas to determine if there was any optic nerve involvement. The patients ranged in age from 6 to 34 years. Visual acuity ranged from 20/20 to 20/100. Nineteen eyes of 12 patients (79%) had abnormal (mean +/- 3 S.D.) pattern reversal visual-evoked potentials as compared to 50 control eyes (P100 = 98.8 msec; S.D., +/- 4.5 msec). P100 latency appeared to worsen with age. Exodeviation was present in seven patients (58%) and correlated with visual acuity and P100 latency. Ophthalmoscopic examination showed some degree of optic nerve pallor in all eyes.

Adolescent↗
PubMed1987

Effects of substance P, neurokinin A and calcitonin gene-related peptide in human skin and their involvement in sensory nerve-mediated responses.

The effects evoked by intradermal injections of substance P (SP), neurokinin A (NKA) or calcitonin gene-related peptide (CGRP) were studied in 51 non-atopic subjects. SP and NKA produced flare and weal, and CGRP produced an indurated erythema. The reactions to SP were strong, the flare being maximal 3-5 min after injection and the weal after 10-15 min. NKA evoked a much weaker flare and a slightly weaker weal than did SP. CGRP produced a prominent long-lasting, indurated erythema with pseudopodia surrounded by a pallor edge. The mode of action of the three peptides was studied by pretreatment of the skin with the histamine-releasing compound 48/80, the H1-antagonist mepyramine or the local anesthetic xylocaine. The results suggest that mast-cell histamine and an intact sensory nerve supply are essential for the flare response to both SP and NKA. The weal response to SP was somewhat reduced by pretreatment with either 48/80 or xylocaine. The weal response to NKA, however, did not seem to depend upon either mast cells or sensory nerve fibres. The erythema evoked by CGRP was not suppressed by pretreatment with xylocaine, compound 48/80 or mepyramine, suggesting a direct action of CGRP on the blood vessels. The interaction between SP and CGRP was studied in subjects receiving a low dose of CGRP and increasing doses of SP or a low dose of SP and increasing doses of CGRP. CGRP did not potentiate the SP-evoked flare and weal and SP did not seem to enhance the response to CGRP.

Adult↗
PubMed1984

The involvement of melanotrophins in physiological colour change in the dogfish Scyliorhinus canicula.

Desacetylated alpha-, beta-, and gamma-MSH purified from the neurointermediate lobe of the pituitary gland of the dogfish Squalus acanthias were all equipotent in turning partially hypophysectomized dogfish, Scyliorhinus canicula, dark. However, each possessed less than 2% of the melanotrophic activity of either acetylated mammalian alpha-MSH or synthetic acetylated Squ. acanthias alpha-MSH. These results suggest that acetylation is much more important than amidation in determining melanotrophic potency in vivo in the dogfish. Intravenous administration into grey-adapted dogfish of an antibody capable of binding the alpha-MSH-like peptides present in the blood was very effective at inducing pallor. In contrast, a gamma-MSH antibody had no effect on the melanophores of Scy. canicula. Overall the results suggest that it is alpha-melanotrophins that regulate physiological colour change in the dogfish Scy. canicula.

Acetylation↗
PubMed1986

Effects of catecholamines on plasma thyroid hormone levels in arctic charr, Salvelinus alpinus.

Plasma levels of L-thyroxine (T4) and 3,5,3'-triiodo-L-thyronine (T3) were measured in arctic charr at 2, 6, or 24 hr after single intraperitoneal injection of epinephrine (E) or norepinephrine (NE). At a dose of approximately 1 microgram/g body wt (sufficient to cause a submaximal dermal melanophore pallor response) plasma T4 was usually elevated at 2 hr, consistently depressed at 6 hr, and unaffected at 24 hr. There was no effect of E on plasma [125I]T4 kinetics or [125I]T4 5'-monodeiodination to [125I]T3. Plasma T3 showed no consistent response to E or NE at any sampling time. At an E dose of 4 ng/g body wt (probably sufficient to cause a physiological elevation in plasma E level), neither plasma T4 nor T3 levels were altered at 6 hr. Acute depression in plasma T4 by the high doses of E and NE may reflect a local neurotransmitter role of catecholamines in inhibiting thyroidal T4 release through action at thyroidal, hypophysial, or hypothalamic levels.

Animals↗
PubMed1987

Melanin concentrating hormone inhibits the release of alpha MSH from teleost pituitary glands.

A radioimmunoassay was developed for salmonid melanin concentrating hormone (MCH) and used to measure immunoreactive (ir)MCH in the hypothalamus and pituitary of trout (Salmo gairdneri) and eels, (Anguilla anguilla) maintained under different regimes of background color. In trout, 95% of the total irMCH was located in the pituitary gland. The amount of MCH in both pituitary and hypothalamus was increased when white-adapted trout were transferred to a black background. In eels, a similar change of background led to an accumulation of MCH in the pituitary but not in the hypothalamus. The results suggest that MCH is released from the neurohypophysis in association with physiological color change. Neurointermediate lobes of trout and eels released both ir alpha MSH and irMCH when they were cultured in vitro. The release of alpha MSH was significantly enhanced when endogenous MCH was immunoabsorbed by MCH antiserum added to the culture medium. The results indicate that MCH can induce pallor in fish not only by its peripheral effect on the melanophores but also by an inhibitory action on the release of alpha MSH from the pituitary.

Anguilla↗
PubMed1984

Comparisons between different syndromes of heart attack--a multivariate analysis.

A register of acute coronary events in Auckland, New Zealand enabled characterization of cases of the following different coronary syndromes: definite myocardial infarction (MI) (divided to Type I with typical ECG findings and Type II with new symmetrical T wave inversion only), nonhypotensive definite infarction with and without ventricular fibrillation, possible myocardial infarction and sudden death. Comparisons between these syndromes were analyzed. ECG type II (as compared to ECG type I) definite infarction was a more chronic, repeated syndrome, with more myocardial fibrosis in fatal cases, and more previous prolonged anginal pain without documented infarction. Cases of possible (as compared to definite) myocardial infarction were also more likely to report previous prolonged aningal pain, to use beta blockers, furosemide and less likely to die within 30 days. They consumed significantly more alcohol and were more likely to be female, than cases of definite infarction. Patients with nonhypotensive definite infarction complicated by ventricular fibrillation had higher acute phase pulse rates and more pallor and sweating than similar patients not experiencing ventricular fibrillation. Some possible explanations for the above findings were discussed.

Analysis of Variance↗
PubMed1981

Experimental potassium depletion myopathy.

Myopathic morphological changes were observed in the calf muscles of rats maintained on a potassium-depleted diet for 30-50 days. Light-microscopic changes were more severe in the superficial gastrocnemius muscle fibres and included pallor, swelling and vacuolation, progressing to necrosis, mononuclear cell infiltration and phagocytosis. Mitochondrial disruption, transverse tubular dilatation, membranous body formation and vacuolation were seen on ultrastructural examination. Both vacuoles and subsarcolemmal membranous bodies were shown to be in continuity with the transverse tubular system. More advanced myopathic changes were those of sarcomere destruction and muscle fibre necrosis. Morphological changes resemble those of human potassium depletion myopathy. Ineffective energy metabolism and focal ischaemia due to impaired vasodilatation are proposed as mechanisms for the myopathy of potassium depletion.

Animals↗
PubMed1989

Glial cytoplasmic inclusions in the CNS of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome).

Glial cytoplasmic inclusions (GCIs) were demonstrated by silver staining, immunocytochemistry and by electron microscopy in the central nervous system (CNS) of 11 patients with various combinations of striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome. Although their configuration in light microscope can sometimes resemble neurofibrillary tangles, their cellular localisation, measurements, ultrastructure, immunocytochemical characteristics and regional distribution all differ from these Alzheimer type changes. The majority of GCIs were localized in the white matter and appeared to be accompanied by an increase in the number of interfascicular oligodendroglial cells and pallor or loss of myelin staining. Our histological, ultrastructural and immunocytochemical findings all indicate that the cells which contain GCIs are oligodendrocytes and the inclusions themselves are composed of tubular structures. The presence of the until now unknown GCIs in all the 11 CNS, but not in age- and sex-matched control brains, indicates that GCI is a cellular change characteristic of multiple system atrophy and the three syndromes are various manifestations of the same disease.

Adult↗
PubMed1990

Pathology of chronic myelopathy associated with HTLV-I infection (HAM/TSP).

The CNS pathology of 10 autopsy cases of Japanese HAM/TSP patients with a serological confirmation of HTLV-I infection was reviewed. The essential histopathological feature was a chronic progressive inflammatory process with marked parenchymal exudation of lymphocytes and monocytes into both the grey and white matter of the spinal cord, uniquely perpetuating for more than 3 years after the onset of neurological symptoms, and resulting in severe degeneration of the white matter accompanied by marked glio-mesenchymal tissue reactions. Both the inflammation and the white matter degeneration were most conspicuous in the lower thoracic cord. The lateral column was always and most severely affected. Although the parenchymal tissue degeneration was not confined to any particular long tracts, symmetrical degeneration of the lateral pyramidal tract was evident in all cases. Diffuse myelin pallor was also seen in the anterior column but it was usually mild. The posterior column was commonly involved but the severity and extent of the white matter degeneration were variable. Neurons were relatively well preserved. These histopathological features of HAM/TSP in Japan largely agree with those previously described for HAM/TSP in tropical regions. In the absence of detectable amount of HTLV-I antigens at the sites of inflammation, "chronic progressive parainfectious myelitis" seems to be the most appropriate descriptive term for this unique histopathology of HAM/TSP.

Aged↗
PubMed1991

Traumatic brain injuries: structural changes.

A host of complications and consequences may follow a contusion or other brain injury of any sort. An appreciation of the temporal evolution of the contusion from a microscopic standpoint is useful to a full understanding of the process by which physical force damages the brain and how the brain reacts to this damage. Some disruptions of the blood brain barrier quite early will result in extracellular edema. The microscopic appearance of an edematous area is usually spongy with numerous vacuoles. The neuropil may appear bubbly, and glial cells may be swollen. If edema has been long standing, the vacuoles may be larger and in fact a small cyst may appear in the white matter. If focal cerebral edema is not present for long periods of time and the underlying cause has been corrected, residual fluid and electrolytes are eventually removed, restoring the neuropil to a normal state, leaving no sign of its presence. However, in longer standing lesions, myelin pallor and some reactive gliosis may remain indefinitely. Neurons may show swelling very early and for a short period of time, which gives way to shrinkage, eosinophilia, and nuclear pyknosis. These changes may be observed at the periphery of lesions for as long as 5 or 6 months after the initial event. Before dissolution, nuclear pyknosis may remain in the tissue for many days and possibly longer, and may even become mineralized in situ (ferruginated neurons) to remain for years. In a traumatic lesion, swollen and ballooned axons may be found in and around the contusion but also at great distances from it (diffuse axonal injury). Axonal ballooning may be observed between 24 and 48 h postinjury and may persist wherever found for many years. Selective axonal calcification has been observed in humans as well as in experimental trauma. At about 7-10 days postinjury increased numbers of astroglia probably are present. Over the ensuing weeks and months, and probably years, astrocytes increase in number and in fibrillary appearance, eventually resulting in a glial scar in and about the injured area. It is thought that this reactive gliosis results in restoration of the blood-brain barrier in the damaged area.

Astrocytes↗
PubMed1994

Involvement of the central nervous system in myotonic dystrophy.

To investigate the etiological factors responsible for intellectual impairment and mood changes in patients with myotonic dystrophy (DM), we evaluated 14 patients with DM by means of neuropsychological evaluation and magnetic resonance images (MRI). There were significant differences between patients and controls in regard to the Barthel index, Zung's depression scale, attention, verbal fluency and digit span. All patients had ventricular enlargement and white matter abnormalities on MRI. However, the severity was variable and there was no difference in neuropsychological testing between patients with mild ventricular dilatation and those with severe dilatation. On the other hand, significant differences were present between patients with mild white matter lesions and those with severe white matter abnormalities in regard to verbal fluency and attention. Neuropathologic examination of an autopsied brain showed an increase in the interfascicular space of the white matter which produced pallor on myelin staining. The present findings suggested that the white matter abnormalities were the cause of cognitive impairment among patients with DM.

Activities of Daily Living↗
PubMed1983

Human tolerability studies with D-Met2,Pro5-enkephalinamide.

As reported previously D-Met2,Pro5-enkephalinamide (EA) is a highly active enkephalin analogue. To examine its human tolerability male volunteers were treated s.c. with increasing doses (0.1-30.0 mg). The observed autonomic effects were as follows: feeling of heaviness in the limbs, dry mouth, pallor of the face and conjunctival injection. There was no significant change in blood pressure, pulse and respiratory frequency. The autonomic effects appeared within 15-30 min. However, its effects on mood and wakefulness i.e. slight drowsiness, decrease in psychic tension and emotional detachment developed only later. The serum prolactin level increased dose-dependently, while the growth hormone (HGH) content showed biphasic dose-response pattern. The TSH content increased only at the highest doses applied (10.0-30.0 mg).

Adult↗
PubMed1989

Melanin concentrating hormone. I. Influence of nerves and hormones on the control of trout melanophores.

When melanophores on trout scales are cultured in vitro they show a transitory melanin concentration, which can be prevented by addition to the medium of the alpha adrenergic blocker, phentolamine. This indicates the release of endogenous nor-epinephrine from local nerve terminals. This initial phase of melanin aggregation is followed by redispersion and then by a second, more gradual melanin concentration over several days, which is not antagonized by phentolamine. A final melanophore index of between 2-2.5 is attained which may be the resting state of trout melanophores. Using short-term cultured melanophores which have passed the phase of endogenous nor-epinephrine release, it is shown that exogenous nor-epinephrine will interact synergistically with the melanin-concentrating hormone to achieve full melanin concentration. Evidence is discussed for believing that in the trout, such synergy is necessary to achieve maximum pallor in vivo.

Animals↗
PubMed1991

The background adaptation of the flatfish, Paralichthys olivaceus.

The background adaptation of the flatfish, Paralichthys olivaceus, was studied by sliding beneath the fish a long strip of plastic sheet with various patterns to serve as a background. The body shade and pattern differed depending upon the pattern used. In general, the fish showed maximal pallor on a white background and darkened when lying on a black background. With a pattern of large checks, several black patches became conspicuous. The fish showed the same tendency in terms of response even when the left eye was covered. However, the fish was prevented from manifesting these changes when the right eye was covered. The results suggest that the left eye of the fish does not see the immediate background. This conclusion is supported by an anatomical study.

Animals↗
PubMed1993

Anaemia in housed lambs.

Anaemia was detected in housed lambs by clinical and haematological investigation. Conjunctival pallor was used as a clinical test for anaemia and the results indicate that this has high specificity (91 per cent to 95 per cent) and low sensitivity (53 per cent to 55 per cent). The haematological results indicated a non-regenerative anaemia with low packed cell volume, red blood cell count and haemoglobin. In a subset of lambs examined biochemically, anaemia was associated with low serum iron concentration and low serum iron binding: cobalt levels were within normal ranges and blood copper levels were slightly raised. At present it is unclear whether this is a primary or secondary iron deficiency.

Anemia↗
PubMedDate not supplied

Hemeralopia in an older adult.

An elderly male was referred for evaluation of hemeralopia when cataract extraction did not alleviate his symptom of difficulty seeing in bright illumination. Visual acuity was 20/40 OU. Funduscopic examination revealed marked arteriolar attenuation, disc pallor, and retinal pigment epithelial changes. Visual fields demonstrated relative paracentral scotomata. An ERG was consistent with widespread photoreceptor degeneration. A diagnosis of visual paraneoplastic syndrome was made and an extensive systemic evaluation revealed a squamous cell carcinoma of the lung. The presentation and evaluation of acquired photoreceptor dysfunction in adulthood is discussed.

Aged↗
PubMedDate not supplied

Optic nerve enlargement and chronic visual loss.

We present four patients with sarcoidosis of the anterior visual pathways. The first patient presented with unilateral visual loss, a mass lesion at the optic nerve head, and an enlarged orbital optic nerve. The second patient presented with bilateral progressive painless visual loss, associated with optic nerve pallor and visual field loss. In these two patients, optic nerve biopsy was diagnostic of sarcoidosis. The third patient developed optic nerve and chiasmal involvement after sarcoidosis was established by lacrimal gland biopsy. The fourth patient had optic nerve, pulmonary, and lymph node involvement with sarcoidosis. A conjunctival and lung biopsy were diagnostic. Computed tomography and magnetic resonance imaging have greatly facilitated diagnosis of sarcoidosis of the anterior visual pathways. Sarcoidosis of the anterior visual pathways may occur alone or in association with other ocular or systemic manifestations. A conjunctival or lacrimal gland biopsy may be preferable as the initial diagnostic approach. Treatment of patients with this condition may require systemic immunosuppression, in addition to corticosteroids, to prevent permanent visual loss.

Adult↗
PubMedDate not supplied

Is all nondefinable optic atrophy Leber's hereditary optic neuropathy?

Leber's hereditary optic neuropathy has been considered a bilateral, sequential hereditary optic neuropathy occurring overwhelmingly in young men. Until recently the diagnosis has been based on clinical criteria: severe loss of vision associated with central scotomas and classic ophthalmoscopic findings (circumpapillary telangiectatic microangiopathy, pseudoedema of the disk with absence of staining on fluorescein angiography, tortuous vessels in the early stages and eventually optic disk pallor). In 1988 a genetic mutation associated with Leber's hereditary optic neuropathy affecting mitochondrial DNA was recognized. Subsequently other mutations have been discovered as well. The ability to identify these patients technically has allowed us to recognize cases that do not fit our previous clinical criteria. One such case is presented and the question asked is whether the findings are related to the clinical course.

Child↗