Müller's Muscle Research Articles

Distribution of adrenergic nerves in the eye and some related structures in the cat.

AbstractWith the specific and highly sensitive fluorescence technique of Falck and Hillarp, the distribution of adrenergic nerves has been studied in the eye and some related structures in the cat. Adrenergic nerves occur in the cornea, in the loose connective tissue at the limbus, in the tissues of the chamber angle and in the iridic stroma. The large vessels of the iris possess the same spacious arrangement of the adrenergic fibres as is seen in many other mammals. Both the sphincter and the dilator pupillae have a rich supply of varicose adrenergic fibres. There is a layer of varicose adrenergic fibres under the ciliary epithelium and in the ciliary processes. In the retina, there is a layer of adrenergic fibres between the inner nuclear and the inner plexiform layers, as well as adrenergic nerve cells both in the inner nuclear layer and ganglion cell layer. The tarsal muscle as well as the muscle of the nictitating membrane has a wide‐meshed plexus of adrenergic nerves. In the lacrimal gland, seemingly every secretory cell is reached by an adrenergic fibre.

Studies of thyroid and sympathetic nervous system interrelationships. I. The blepharoptosis of myxedema.

Blepharoptosis (drooping of the upper eyelid) was observed in 20 of 27 patients (74 per cent) with untreated myxedema of various types and in 6 of 18 myxedematous patients (33 per cent) treated with desiccated thyroid. The blepharoptosis was characteristically of modest degree and could bo overlooked easily. Lid edema, although frequent, was not always associated with ptosis. The tarsal fold was intact and normal voluntary and conjugate lid elevation was possible. Phenylephrine hydrochloride, when instilled into the conjunctival sac, corrected the ptosis in all cases. Electromyograms of the levator palpebrae superioris muscles were normal in 4 patients. Urinary catecholamine excretion was normal in 4 patients. Intravenous infusion of epinephrine did not correct the ptosis in 6 patients. The evidence suggests that blepharoptosis in myxedema results primarily from diminished tone of the sympathetic nerve fibers to Muller's superior palpebral muscle rather than from an abnormality of the levator palpebrae su...

Horner's syndrome: roentgen manifestations.

Hare (1) in 1838 and Horner (2) in 1869 described the group of clinical symptoms now known as Horner's syndrome. It consists of miosis, ptosis of the upper lid, enophthalmos, dryness of the skin of the face, and vascular hyperemia. In progressive cases, paresthesia of the arm follows, succeeded in turn by muscular atrophy. All symptoms are ipsilateral. This syndrome is produced by damage to the cervical sympathetic or to part, or all, of its ganglia at the eighth cervical or the first two thoracic levels, the severity of the manifestations depending on the extent of the lesion. The same symptoms may be the result of damage to the ciliospinal center of the spinal cord at the appropriate levels or to the roots extending from those parts of the cord. Causative lesions include neoplastic invasion of the nerve sheaths or walls of the arteries and secondary degenerative changes produced by pressure. The etiologic factors in the development of Horner's syndrome and the clinical data may be summarized as follows: Horner's Syndrome: Clinical and Etiologic Factors I. Symptoms (all ipsilateral) 1. Miosis, paralysis of the dilator pupillae 2. Ptosis of the upper lid, paralysis of the tarsal muscle 3. Enophthalmos, paralysis of the orbital muscle (Müller) 4. Anhidrosis of the skin of the face 5. Vascular hyperemia of the face 6. Paresthesia of the arm followed by muscular atrophy (Klumpke syndrome) II. Pathology 1. Damage to the cervical sympathetic or part or all of its ganglia, at the level of C-8, D-l, and D-2 2. Damage to the ciliospinal center of the spinal cord at the same level 3. Damage to roots above mentioned neurons and their communicating branches III. Causes (producing pressure and degeneration or direct invasion and destruction of the neurons)* 1. Congenital Status dysraphicus, cervical rib, congenital spine deformities (r.d.) 2. Inflammatory: Herpes zoster (c,d.) Tuberculosis, osseous or glandular, level of C-8, D-l, and D-2 (r.d.) Syphilis: aneurysm (c.d. and r.d.) Epidemic meningitis (c.d;) Encephalitis (c.d.) Anterior poliomyelitis (c.d.) 3. Traumatic Postoperative complications, pneumolysis, gun and knife wounds, thoracotomies, paravertebral block, phrenicotomy, hematomyelia; level of C-8, D-l, and D-2 (c.d. and r.d.) 4. Degenerative Bulbar palsy, syringomyelia (c.d.), scleroderma (Bing, ) (c.d.) 5. Neoplastic Lymphosarcoma, Hodgkin's disease (c.d. and r.d.) Neurofibrosarcoma, epipharyngeal carcinoma (Bremer) (c.d. and r.d.) Thymoma, struma maligna (c.d. and r.d.) Bronchogenic carcinoma with soft-tissue metastases at level of C-8, D-l, D-2 (no bone destruction) (c.d. and r.d.) Pancoast tumor, with bone destruction (r.d. and c.d.) Metastases to soft tissues and bone from distant neoplasms (r.d. and c.d.) Tumor of the gasserian ganglion (c.d.) Of the congenital conditions which may produce Horner's syndrome special mention may be made of “status dysraphicus.”

Sympathetic innervation of the heart in man: Preliminary observations of the effect of thoracic sympathectomy on heart rate: Chapman, E. M., Kinsey, D., Chapman, W. P., and Smithwick, R. H.: J. A. M. A. 137:579 (June 12), 1948

The developmental influence of sympathetic innervation on parasympathetic nerve density was investigated in the tarsal smooth muscle of the rat. Specificity of acetylcholinesterase staining as a marker for parasympathetic innervation was first determined by acute selective denervations. Excision of the ipsilateral superior cervical ganglion caused a 39% reduction in the density of acetylcholinesterase-positive nerves seven days later, indicating that sympathetic nerves contribute to cholinesterase-positive tarsal muscle innervation. Excision of the pterygopalatine ganglion concurrent with superior cervical ganglionectomy caused a virtually complete disappearance of acetylcholinesterase-positive innervation within seven days, indicating that non-sympathetic cholinesterase-positive fibers derive from the pterygopalatine ganglion and are presumed to be parasympathetic. Analysis of the control population indicated that parasympathetic nerve density did not vary significantly between males and females, between the superior and inferior muscles, or in rats studied at four and 12 months of age. The influence of sympathetic innervation on parasympathetic nerve density during postnatal development was examined by conducting surgical sympathectomies on postnatal day 5 and quantifying acetylcholinesterase-positive nerve density at four months of age. Neonatal sympathectomy caused a 46% reduction in cholinesterase-positive nerve density beyond that which occurred in acutely sympathectomized adult controls.It is concluded that sympathetic innervation is required for developing parasympathetic nerves to attain their normal density within the rat tarsal muscle. This finding is consistent with the idea that sympathetic nerves can exert positive effects on parasympathetic nerve outgrowth during development.

Sympathectomy for essential hypertension: Fishberg, A. M.: J. A. M. A. 137:670 (June 19), 1948

The developmental influence of sympathetic innervation on parasympathetic nerve density was investigated in the tarsal smooth muscle of the rat. Specificity of acetylcholinesterase staining as a marker for parasympathetic innervation was first determined by acute selective denervations. Excision of the ipsilateral superior cervical ganglion caused a 39% reduction in the density of acetylcholinesterase-positive nerves seven days later, indicating that sympathetic nerves contribute to cholinesterase-positive tarsal muscle innervation. Excision of the pterygopalatine ganglion concurrent with superior cervical ganglionectomy caused a virtually complete disappearance of acetylcholinesterase-positive innervation within seven days, indicating that non-sympathetic cholinesterase-positive fibers derive from the pterygopalatine ganglion and are presumed to be parasympathetic. Analysis of the control population indicated that parasympathetic nerve density did not vary significantly between males and females, between the superior and inferior muscles, or in rats studied at four and 12 months of age. The influence of sympathetic innervation on parasympathetic nerve density during postnatal development was examined by conducting surgical sympathectomies on postnatal day 5 and quantifying acetylcholinesterase-positive nerve density at four months of age. Neonatal sympathectomy caused a 46% reduction in cholinesterase-positive nerve density beyond that which occurred in acutely sympathectomized adult controls.It is concluded that sympathetic innervation is required for developing parasympathetic nerves to attain their normal density within the rat tarsal muscle. This finding is consistent with the idea that sympathetic nerves can exert positive effects on parasympathetic nerve outgrowth during development.

FRACTURES OF THE ORBITAL FLOOR

In this paper I shall describe a not infrequently neglected deformity, present typical case reports of the condition in its various degrees of extent, evaluate the various methods of treatment which have been advocated and describe in detail the treatment which has proved most satisfactory in a group of 34 patients. Lukens¹, reviewing the literature forty years ago, found 78 cases of traumatic enophthalmos and some nineteen hypotheses to explain its mechanism. Among the etiologic factors suggested were: (1) indirect fracture of the orbital walls, (2) direct fracture of the orbital walls, (3) injury to Muller's orbital muscle, (4) injury to the check ligaments, (5) rupture of Tenon's capsule, (6) atrophy of orbital tissue due to injury of the sympathetic or trigeminal nerves, (7) hemorrhage of the ophthalmic artery behind the ciliary body, (8) minute hemorrhages in the nerve sheaths, particularly of the sympathetic nerves, (9) cicatricial contraction of

NEURON PATTERNS CONTROLLING TRANSMISSION OF IPSILATERAL HIND LIMB REFLEXES IN CAT

NEURON PATTERNS CONTROLLING TRANSMISSION OF IPSILATERAL HIND LIMB REFLEXES IN CAT

EXOPHTHALMOS IN PATIENTS WITH VARIOUS TYPES OF GOITER

Exophthalmos may be defined as protrusion of the globe of the eye. It occurs in diseases of the thyroid, sinusitis, intracranial arteriovenous aneurysms, benign or malignant tumors (either primary or metastatic) of the orbit or within the cranial vault, thrombosis of the cavernous sinus, myopia, xanthomatosis, congenital malformations of the skull, Paget's disease and other diseases of the bones and hypertension. It rarely appears as voluntary exophthalmos. The discussion in this paper will be limited to the exophthalmos that occurs in certain types of disease of the thyroid. The mechanism of the exophthalmos associated with spontaneous or experimentalthyrotoxicosis varies because of the anatomic peculiarities of different species of animals. In animals other than man stimulation of the cervical sympathetic nerves causes protrusion of the eyeball by contraction of Muller's muscle. 1 Although in man Muller's muscle is vestigial, many studies have been made concerning the role of cervical sympathetic stimulation

Designing the longest fixed steel arch : D B. Steinman and C. H. Gronquist. (Engineering News Record, Vol. 117, No. 7.)

As a thin filmy covering overlaying the inferior orbital fissure (IOF), Muller's muscle was considered a vestigial structure in humans, and for this reason, its anatomical significance was neglected. Because of increasing interest in endonasal approaches to the skull base that encompasses this region, we re-examined this structure's role as an anatomical landmark from an endoscopic perspective.In 10 cadaveric specimens, microanatomical dissections were performed (n = 5); endoscopic dissections were performed (n = 5) via approaches of the middle turbinate or inferior turbinate, and via the Caldwell-Luc approach through the maxillary sinus. Histological examinations were performed in 20 human fetuses (Embryology Institute, Universidad Complutense de Madrid, Madrid, Spain).In cadaveric dissections, Muller's muscle was demonstrated in all specimens, serving as a bridge-like structure that spanned the entire IOF and separated the orbit from the temporal, infratemporal, and pterygopalatine fossas. Depending on which endoscopic corridor was used, a different aspect of the IOF and Muller's muscle was identified. In our endoscopic and microscopic observations, Muller's muscle was extensive, not only spanning the IOF but also extending posteriorly to reach the superior orbital fissure (SOF) and anterior confluence of the cavernous sinus. Histological analysis identified many anastomotic connections between the ophthalmic venous system and pterygoid plexus that may explain how infection or tumor spreads between these regions.Muller's muscle serves as an anatomical landmark in the IOF and facilitates anatomical orientation in this region for endoscopic skull base approaches. Its recognition during endoscopic approaches allows for a better three-dimensional understanding of this anterior cranial base region.

EXPERIMENTAL PTOSIS IN PRIMATES

The upper eyelid is raised by the action of the levator palpebrae superioris and Muller's palpebral muscle. The former is innervated by the oculomotor nerve and the latter by fibers from the cervical portion of the sympathetic trunk. Ptosis of the upper lid follows paralysis of either nerve supply, that due to a lesion of the oculomotor nerve being greater than the slight droop which is seen in Horner's syndrome1due to involvement of the cervical portion of the sympathetic trunk (figure,A). Likewise, there is limitation of the upward excursion of the lid when the eyeball is elevated in disorders referable to the oculomotor nerve while in disturbances of the sympathetic innervation the amplitude is normal. With section of the third nerve mydriasis occurs as well as external and internal ophthalmoplegia, while a lesion of the sympathetic trunk causes miosis and enophthalmos. This communication deals with ptosis produced

PATHOLOGY OF THE CERVICAL SYMPATHETIC.

The departure from the normal in the cervical sympathetic may be classed under two heads, namely, irritation and paralysis. 1. The symptoms of irritation are: (a) mydriasis, due to spasm of the dilator pupillae; (b) exophthalmus, said to be due to contraction of the smooth muscular fibers of the orbit (Muller's); (c) widening of the palpebral fissure by tonic contraction of Muller's muscle; (d) contraction of the walls of the vessels of the head, face and neck, including pallor of the skin, frequently with an increase in the amount of perspiration; (e) acceleration of the heart beat. According to Nicati,1paralysis of the cervical sympathetic may be divided into two stages: First Stage. —(a) Contraction of the pupil, (b) narrowing of the palpebral fissure (ptosis), (c) decrease of the tension of the globe, (d) increased lachrymation, (e) injection of the ocular conjunctiva, and, in many cases, (f) slight exophthalmus.

THE VOLUNTARY AND INVOLUNTARY BRAIN CENTERS CONTROLLING THE OCULAR MUSCLES.

There are two groups of brain centers for controlling the movements of the eyes. One group is found in the cortex, and consists of nine distinct centers. In this group are two more centers, making eleven in all, but these two are connected with muscles within the eye, viz. : the Muller muscle in the ciliary body and the sphincter of the iris, and will not be specifically studied in this paper. The second group is located at the base of the brain, and consists of twelve distinct centers. In this group are four more centers, making sixteen in all, but these four are connected with the muscles within the globe already mentioned, hence they will be passed without further mention. THE CORTICAL GROUP. Experimentation and pathology both have given evidence of the existence of the cortical centers. Experimenters on the lower animals have not yet found