Biomedical subjects
Publications and source records attributed to S W Carmichael.
Compression of the ulnar nerve can be understood in terms of the anatomic and dynamic factors. Although the ulnar nerve may be compressed at any point along its course, it is particularly susceptible at the elbow and the wrist. Clinically relevant anatomy will be reviewed in an attempt to provide the reader with a logical framework for successfully diagnosing and managing typical and atypical ulnar nerve compression lesions.
The morphological characteristics of shoulders with torn rotator cuffs were determined using 41 embalmed specimens. The following parameters were measured in the supraspinatus (SSP), infraspinatus (ISP) and subscapularis (SSC) muscles: the length, thickness and width of the extramuscular tendon; the length of the intramuscular tendon; the length and width of a tear, if present, muscle fibre length; and muscle volume. The cross-sectional area (CSA) of the tendon was measured on the photographic image of slices of the tendon using an image analysis system, and the CSA of the muscle was calculated by dividing the muscle volume by muscle fibre length. The rotator cuff was intact in 11 shoulders. A partial-thickness tear of the cuff was present in 12 shoulders, a full-thickness tear of the SSP in 11 shoulders, and a full-thickness tear of more than 2 tendons in 7. Overall incidence of full-thickness tears of the rotator cuff was 44%, and that of partial-thickness tears 29%. With increase of tear size, the functional tendon length (extramuscular tendon length plus tear length) increased by a statistically significant amount in the SSP, ISP and SSC, whereas muscle fibre length decreased in SSP and ISP. It is concluded that the increased functional tendon length and decreased muscle fibre length are the main morphological changes that make the rotator cuff a physiologically abnormal unit. Surgical repair of the torn cuff would be expected to improve these anatomical changes and restore the kinetics of the glenohumeral joint.(ABSTRACT TRUNCATED AT 250 WORDS)
Parkinson's disease has been described as a multisystem disorder that includes alterations in the function of the autonomic nervous system. The activity of the adrenal medulla in this disease has not been thoroughly investigated. Previous reports are reviewed that demonstrate that the adrenal medullae of parkinsonian patients are compromised, having a decreased content of all catecholamines and several neuropeptides. An animal model was used to investigate whether the observations made in human patients were related to extended treatment with antiparkinsonian medications or were a natural concomitant of the disease. Administration of L-dopa and/or carbidopa to C57BL mice for 4-16 weeks had no significant effect on the level of any of the adrenal medullary catecholamines. Treatment with MPTP 4-16 weeks prior to sacrifice did not deplete adrenal medullary catecholamines in these animals, thus not fully mimicking Parkinson's disease in this animal model. The only significant effect was an interaction between group (MPTP or control) and treatment with antiparkinsonian medications; L-dopa, in the absence and presence of carbidopa, had opposite effects in the two groups. Based primarily on the lack of effect of antiparkinsonian medications on adrenal medullary catecholamines, it was concluded that the adrenal medullary depletion observed in human patients was a peripheral concomitant of Parkinson's disease.
The boundaries of Guyon's canal have recently been redefined by a series of anatomical dissections. These showed that the confines of this space do not extend from the pisiform to the hook of the hamate, as currently accepted. The fascial roof extends radial to the hook of the hamate, which allows the ulnar neurovascular bundle to course radial to the hamate hook. The position of the ulnar nerve and artery is of particular significance for endoscopic carpal tunnel release. Most endoscopic devices are designed to divide the flexor retinaculum just to the radial aspect of the hamate hook. Utilizing cross-sectional analysis of nine cadaver specimens, we found the ulnar artery to course radial to the hamate hook in five and palmar to it in four. Therefore, the ulnar artery may be at greater risk of injury during endoscopic procedures than previously recognized.
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The anatomical characteristics of the flexor carpi radialis tendon, the tendon sheath, the tunnel boundaries, and the adjacent structures were examined in twenty-five adult cadaveric specimens. Transverse and sagittal sections of the wrist and forearm, tenograms, and histological sections of the tendon were made from two additional specimens each. The musculotendinous portion of the flexor carpi radialis tendon begins an average of fifteen centimeters (range, twelve to seventeen centimeters) proximal to the radiocarpal joint; the muscular fibers end an average of eight centimeters (range, six to nine centimeters) proximal to the wrist. The synovial sheath extends from the origin to the insertion. The tendon enters a fibro-osseous tunnel at the proximal border of the trapezium and is separated from the carpal canal by a thick septum that functions, at its distal border, as a pivot point for the flexor pollicis longus. Within the tunnel, the tendon occupies 90 per cent of the available space and is in direct contact with the slightly roughened surface of the trapezium. The tendon lies within a few millimeters of the distal aspect of the radius, the scaphoid tubercle, the scaphoid-trapezium-trapezoid joint, and the carpometacarpal joint of the thumb. In most patients, the flexor carpi radialis tendon is inserted at three locations. A small slip is connected to the trapezial crest or tuberosity; 80 per cent of the remaining tendon is inserted on the base of the second metacarpal and 20 per cent, on the base of the third metacarpal. The deep palmar arch is located two to three millimeters distal to the insertion of the tendon.
Reconstruction of the arteries of the foot in patients with severe chronic arterial occlusive disease has become a routine and valuable procedure. However, it is frequently difficult to select the optimal site for the distal arterial anastomosis. In order to determine the most important anatomic variations of foot arteries and the relationship of the dorsalis pedis artery to crossing tendons, the following study was performed in 30 cadaver limbs of 17 persons (9 men and 8 women). Their mean age at death was 69.8 years (range: 42 to 93 years). Methods to evaluate anatomy included anatomic dissection, arteriography, and preparation of corrosion cast models. The latter was performed by injection of liquid plastic and catalyst into the tibial arteries followed by chemical débridement of the soft tissue of the foot. Photographs of the corrosion cast models were taken at various stages of soft tissue dissolution. The dorsalis pedis artery was absent in 6.7% of the cases, and the arcuate artery was absent in 33%. The dorsalis pedis artery arose from the peroneal artery in 6.7%. The dorsalis pedis artery crossed under the extensor hallucis longus tendon at the ankle in 54%, above the ankle in 43%, but below the ankle in only 3%. Our study suggests that the optimal site for the dorsalis pedis artery anastomosis on the foot is the segment distal to the ankle.
The effect was determined of replacing medium inorganic phosphate with thiophosphate on the structure and function of cultured bovine chromaffin cells. Cell cultures were incubated in normal medium containing fetal bovine serum, phosphate free medium or similar medium supplemented with inorganic phosphate or thiophosphate. In contrast to the other media, cells cultured with thiophosphate medium for 3-4 days showed seriously compromised structure and functions. The cells lost 75% of their catecholamine content and their ability to secrete remaining catecholamines in response to nicotine stimulation. Radiolabelled thiophosphate was rapidly taken up by the cells and, in long-term experiments, was incorporated largely into a 97-121 kDa protein band on SDS-PAGE. Additional minor bands were found to a lesser, variable extent. Transmission electron micrographs of cells treated with thiophosphate showed extensive depletion of chromaffin vesicles and disruption of mitochondria, suggesting that the functional damage noted with these cells could be associated with damage to mitochondria. Analysis of general cell metabolic activity by conversion of the dye (3-[3,4-dimethylthiazol-2-yl]-3,5-diphenyltetrazolium bromide) to its formazan derivative indicated increased metabolic activity at early stages of exposure to thiophosphate followed by a decline with continued exposure, supporting the argument for an overall depression of cell metabolism. Uptake of the dye neutral red, which is avidly accumulated by chromaffin cells, was also reduced for cells exposed to thiophosphate. The data suggest that thiophosphate enters chromaffin cells and disrupts energy dependent cell functions, including catecholamine storage and secretion.
Binding of spiperone and 3-quinuclidinyl benzilate (QNB), both labeled with hydrogen 3 (3H), were measured in caudate tissue obtained from 8 living parkinsonian patients at the time of cerebral transplantation. This was clinically homogeneous group of patients. All remained predominantly responsive to levodopa, although with marked disability secondary to clinical fluctuations (short-duration responses) and medication-induced dyskinesias; all were receiving substantial doses of levodopa and 6 of the 8 patients were additionally receiving bromocriptine or pergolide. Binding densities of dopamine D2 receptors, as measured by [3H]spiperone binding, were reduced in this group of patients, compared to caudate specimens from autopsy control subjects. This findings may reflect medication-induced receptor downregulation. Parallel changes occurred with muscarinic cholinergic receptors; [3H]QNB binding was significantly reduced, compared to autopsy control values. This reduction of muscarinic receptors might be due to loss of nigrostriatal terminals that are known to contain muscarinic receptors. Alternatively, muscarinic receptors may have been downregulated by increased corticostriatal glutamatergic input to cholinergic cells, inferred to be present based on the prominent levodopa-induced dyskinesias. Finally, receptor deficits could have been a reflection of more widespread degenerative cerebral disease, although levodopa-refractory symptoms were generally not pronounced in these patients.
Between January 1, 1980, and June 30, 1989, 9 patients (6 males and 3 females) developed ischemic injury to the spinal cord or lumbosacral plexus following 3,320 operations on the abdominal aorta (0.3%). The incidence of this complication was 0.1% (2 of 1,901) after elective and 1.4% (3 of 210) after emergency abdominal aortic aneurysm repair, and 0.3% (4 of 1,209) after repair for occlusive disease. Three of the latter had prior clinical evidence of distal embolization. Eight grafts were bifurcated (aorto-iliac:four, aorto-femoral: three, aorto-ilio-femoral:one). One patient underwent extra-anatomic revascularization. Only two patients had supraceliac aortic cross-clamping and one patient underwent exclusion of both internal iliac arteries. Four patients had hypotension. Early mortality was 22% (two of nine). Severe perioperative complications, mostly due to associated visceral and somatic ischemia and sepsis, were present in seven of the nine patients. The extent and type of the neurologic injury correlated with long-term outcome. Patients with ischemic injury of the lumbosacral roots or plexus had better recovery. Attention to the pelvic circulation and the collateral blood supply is important. Use of gentle technique to prevent embolization, avoidance of hypotension and prolonged supraceliac cross-clamping, revascularization of at least one internal iliac artery, and the use of heparin may decrease but not eliminate paraplegia. Once this unexpected complication occurs, careful neurologic evaluation should be done to localize the lesion and aid prognosis.
Adrenal medullary tissue was collected from parkinsonian patients at autopsy and at the time of autologous transplantation of the adrenal medulla to the caudate nucleus, and from nonparkinsonian patients at autopsy and during nephrectomy. Levels of the following neuropeptides were measured by radioimmunoassay in samples of the medullary tissue: neuropeptide Y (NPY), substance P (SP), [Met]enkephalin ([Met]ENK), vasoactive intestinal peptide (VIP), peptide YY, and bombesin-like immunoreactivity. Regression analysis was used to establish a relationship between patient age, time to organ harvest, and peptide levels in nonparkinsonian tissue. Levels of [Met]ENK, VIP, NPY, and SP were significantly lower in parkinsonian adrenal medullae than that predicted from the control group. These results suggest that the adrenal medulla of a parkinsonian patient is severely compromised, either by the disease process itself or by the antiparkinsonian medications used to treat the symptoms of the disease.
The chondroepitrochlearis muscle is an extremely rare muscle, arising from the pectoralis major, crossing over the neurovascular bundle in the axilla and inserting into the brachial fascia and medial epicondyle of the humerus. This paper presents the first known neurological complication due to the chondroepitrochlearis muscle.
We present a newly described entrapment of the median nerve caused by compression in the distal arm because of an accessory bicipital aponeurosis. It is characterized by the paresis or paralysis of muscles innervated by the anterior interosseous branch of the median nerve--the flexor pollicis longus, the flexor digitorum profundus, and the pronator quadratus--as well as other more proximal median nerve innervated muscles, namely, the pronator teres and flexor carpi radialis. Sensibility is intact. The site of the Tinel's sign in the distal arm and the clinical appearance of an accessory bicipital aponeurosis help to localize the lesion. Electrodiagnostic studies are also important in establishing the site of the entrapment. The clinical and surgical findings are correlated with the internal topography of the median nerve at its site of compression. It is important to differentiate this syndrome from the classic anterior interosseous syndrome and other nerve entrapments at the elbow and arm. Surgical exploration is indicated if there is no clinical or electromyographic improvement in three to four months after the onset of symptoms.
The anatomy of the cubital tunnel and its relationship to ulnar nerve compression is not well documented. In 27 cadaver elbows the proximal edge of the roof of the cubital tunnel was formed by a fibrous band that we call the cubital tunnel retinaculum (CTR). The band is about 4 mm wide, extending from the medial epicondyle to the olecranon, and perpendicular to the flexor carpi ulnaris aponeurosis. Variations in the CTR were classified into four types. In type 0 (n = 1) the CTR was absent. In type Ia (n = 17), the retinaculum was lax in extension and taut in full flexion. In type Ib (n = 6) it was tight in positions short of full flexion (90 degrees to 120 degrees). In type II (n = 3) it was replaced by a muscle, the anconeus epitrochlearis. The CTR appears to be a remnant of the anconeus epitrochlearis muscle and its function is to hold the ulnar nerve in position. Variations in the anatomy of the CTR may explain certain types of ulnar neuropathy. Its absence (type 0 CTR) permits ulnar nerve displacement. Type Ia is normal and does not cause ulnar neuropathy. Type Ib can cause dynamic nerve compression with elbow flexion. Type II may be associated with static compression due to the bulk of the anconeus epitrochlearis muscle.
Adrenal medullas of 2 baboons perfused with formaldehyde/glutaraldehyde and tannic acid were studied by light and electron microscopy. Tissues were postfixed in OsO4. This procedure allows identification of noradrenaline cells on the basis of a selective reaction of glutaraldehyde with noradrenaline vesicles. As positive control for noradrenaline cells, similarly treated mouse adrenal medullas were also examined. Light microscopic examination of thick sections of baboon medullas did not show noradrenaline cells. In contrast, mouse adrenal medullas showed noradrenaline cells scattered in small groups among the much lighter adrenaline cells. By electron microscopy no noradrenaline cells were seen in the baboon medulla while mouse adrenal medullas showed noradrenaline cells with vesicles possessing exceedingly dense cores and light spaces within their limiting membranes. Otherwise, the majority of the baboon chromaffin cells showed chromaffin vesicles which were round or elongated, 150-520 nm in diameter, and heterogenous in electron density. Cytoplasmic densities were occasionally seen attached to the inner aspect of the plasmalemma, particularly along areas close to blood capillaries. These densities could be chromaffin vesicles in the process of exocytosis. This is the first report of exocytotic profiles in a primate medulla. Occasional small vesicle-containing cells also were present. The vast majority of their vesicles were electron dense. Several possible alternatives for the varied catecholamine vesicular osmiophilia, were discussed. It was suggested that this could be attributed to varied concentration of noradrenaline and adrenaline neurohormones among the vesicle population.
Secretion of the adrenal medulla was stimulated in nine cats by insulin-induced hypoglycemia. Levels of catecholamines (mol. wt 153-183), neuropeptide Y (mol. wt 4254) and chromogranin A (mol. wt 48,000) were measured in concurrently collected samples of adrenolumbar venous blood and thoracic duct lymph for up to 4 h following insulin administration. Insulin-induced hypoglycemia elicited an increase in the secretion of catecholamines, which reached peak levels in the adrenolumbar venous plasma at 1.5-2 h and in the lymph at 2.5 h. Although catecholamines were the most numerous measured molecules in the lymph, levels of norepinephrine and epinephrine were 75-250-fold less than those found in the adrenolumbar venous plasma. Neuropeptide Y in the adrenolumbar venous plasma reached peak levels between 1 and 1.5 h; at this time approximately 20% of the peak venous amount was detected in the lymph. Chromogranin A was found in approximately equal amounts in both plasma and lymph; the peak level in the plasma occurred at 1.5-2 h, while that in the lymph was reached at 2-3 h. We suggest that the size of a molecule influences the route it takes following exocytosis from the chromaffin vesicle. Smaller molecules such as catecholamines may pass directly into the circulation, while larger molecules such as chromogranin A may be temporarily sequestered in the interstitial space before passing into the lymph, and hence into the circulation.
Transplantation of adrenal medulla into the caudate nucleus as treatment for Parkinson's disease was performed in eight patients. Although our previous 6-month follow-up revealed early modest improvement, an extension of that follow-up to 1 year disclosed no additional gains in any patient. At the end of 1 year, only one patient could be categorized as moderately improved; three patients were mildly improved, and four patients were unimproved. The rationale for transplanting adrenal medulla was to reestablish a physiologic source of dopamine to the striatum. We measured cerebrospinal fluid (CSF) and plasma catecholamines and metabolites before and after transplantation. Conjugated dopamine (the predominant form of dopamine found in the CSF) and homovanillic acid (the major dopamine metabolite) were modestly and inconsistently increased in the CSF. Conjugated and free epinephrine and norepinephrine, as well as 3-methoxy-4-hydroxyphenylglycol concentrations were not increased in CSF after graft placement, an indication that the adrenal chromaffin cells were no longer producing high levels of these nondopamine catecholamines and metabolites. CSF cortisol concentrations were not increased after transplantation, compared with values from controls, consistent with low numbers of functioning adrenal cortical cells contaminating the graft (or poor survival). Posttransplantation CSF did not induce a neurotrophic effect in cell cultures of 15-day embryonic rat dorsal root ganglion or PC12 (rat pheochromocytoma) cell lines. Survival of samples of patients' adrenal medullary tissue for 2 weeks in tissue culture attested to the viability of the graft at the time of transplantation. The relative concentrations of dopamine to epinephrine or norepinephrine increased in these cultured adrenal medullary cells, presumably because of loss of the glucocorticoid influence on catecholamine synthesis. A wide variety of factors could have contributed to our failure to replicate the earlier impressive results of adrenal-to-brain transplantation reported by others. Continued transplantation studies in animal models of parkinsonism are necessary for better elucidation of these factors.
Bovine adrenomedullary chromaffin (BAMC) cells, cultured in a defined medium, were used to study the mechanisms of toxicity and cellular resistance to the catecholamine neuron toxicants 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+). The viability of the cells was assessed biochemically [cellular catecholamine content and the catalytic activities of tyrosine hydroxylase (TH) and lactate dehydrogenase (LDH)] and anatomically (by electron microscopy). When cultures of BAMC cells were exposed to MPTP or MPP+ for 3 days, a marked loss of cellular catecholamines and TH activity was observed. The addition of an inhibitor of monoamine oxidase (MAO) B (Ro 19-6327), but not MAO A (clorgyline), prevented the toxicity of MPTP but not that of MPP+. In addition, the cellular toxicity of MPP+, but not MPTP, was antagonized by desmethylimipramine, an inhibitor of cellular catecholamine uptake. The toxicity of MPP+ was time dependent, with losses of TH and the release of cellular LDH occurring after 48 h in culture. Catecholamine depletion occurred somewhat sooner, being evident after 24 h of exposure to MPP+. The cellular toxicity of MPP+ was concentration dependent and significantly enhanced by inhibitors of catecholamine vesicular uptake (reserpine, tetrabenazine, or Ro 4-1284). Electron microscopic examination of cells treated with either MPP+, tetrabenazine, or their combination revealed that MPP+ damaged BAMC cells and that this damage was markedly potentiated by the inhibition of vesicular uptake by tetrabenazine. The concentration of glucose in the culture media of untreated cells slowly decreased as a function of time. The rate of glucose consumption was markedly accelerated by MPP+ treatment and the losses in cell TH and the release of LDH into the media were preceded by a 99% depletion of glucose from the media. In cultures not treated with MPP+, lactate accumulated in the media as a function of time. Addition of MPP+ to the media increased the formation of lactate, in a concentration-dependent manner. Reserpine pretreatment further enhanced the production of lactate in response to MPP+. Culturing cells in glucose-free medium greatly potentiated the effects of MPP+ on cellular TH and catecholamines. The toxicity observed after 3 days' exposure of BAMC cells to MPP+ could be prevented when the medium was replaced with fresh medium every 24 h. The effects of glucose deprivation and reserpine were observed to be additive. The ability of MPP+ to affect mitochondrial function is determined by the capacity of the storage vesicle to sequester the pyridinium, acting as a cytosolic "buffer."(ABSTRACT TRUNCATED AT 400 WORDS)