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Biomedical subjects

B M Patten

Publications and source records attributed to B M Patten.

At least 19 recordsLinked to original sources

William A. Hammond, the dynamograph, and bogus neurologic testimony in old New York.

April 25, 1870, court of General Sessions, New York City, Doctor William A. Hammond, neurologist and former Surgeon General of the United States Army, testified at the trial of his patient Daniel McFarland. McFarland had fatally wounded famous journalist Albert Richardson in November of 1869. Dr. Hammond said McFarland suffered from temporary insanity due to cerebral congestion from over use of the brain. Hammond told the jury he had, "devoted the last five years of his professional life exclusively to the study of the mind", and opined that the evidence of cerebral congestion was profound: McFarland's head was hot, and his carotid throbbed. The proof came from the test with the dynamograph machine: McFarland could not keep a pencil still to trace a straight line in the center of a moving piece of paper. The dynamograph, Dr. Hammond assured the jury, measured the power of a man over his will and thus provided "full and decided evidence" there can be no doubt that McFarland "could not control his will". What were the motivations behind the testimony of this famous expert witness? Did bogus neurologic testimony exist in old New York over a century before our time?

Equipment and Supplies↗

Human adjuvant disease: presentation as a multiple sclerosis-like syndrome.

Twenty-six women had a systemic disease with central nervous system (CNS) involvement at a mean age of 39.2 years (range, 23 to 64 years) after receiving silicone breast implants (n = 25) or silicone fluid injections into breasts (n = 1). The median latency period between breast surgery and onset of symptoms was 5.71 years (range, 3 months to 15 years). All patients had evidence of disseminated CNS lesions; 20 patients also had evidence of peripheral neuropathy. Additional problems included myalgia (n = 24), joint stiffness (n = 23), arthralgia (n = 22), sicca complex (dry eyes and dry mouth) (n = 19), headache (n = 16), skin rash (n = 15), joint swelling (n = 14), Raynaud's phenomena (n = 14), fever (n = 13), hair loss (n = 12), allergies (n = 11), sensitivity to sunlight (n = 10), and lymphadenopathy (n = 9). Magnetic resonance imaging brain scans were abnormal in 22 of 26 patients (21, white matter lesions; 1, ischemic lesions; 4, cerebral atrophy). Spinal tap revealed oligoclonal bands in 18 of 23 patients. Visual evoked responses were delayed in 14 of 23 patients, and autodirected antibodies were detected in 16 of 26. Sural nerve biopsy results showed loss of myelinated fibers in 15 of 15. Seventeen of 24 patients (71%) who had implant removal were found to have grossly ruptured implants. We believe our patients had a new syndrome triggered by the foreign material in their body. This syndrome appears as a systemic inflammatory autoimmune disease with central nervous system involvement resembling multiple sclerosis.

Adjuvants, Immunologic↗

Diagnostic value of clinical examination and various imaging techniques for breast implant rupture as determined in 81 patients having implant removal.

To determine sensitivity and specificity of magnetic resonance imaging (MRI) and ultrasonography (US) in the detection of breast implant rupture, and also to determine the relative merits of clinical examination and mammography, we studied 81 patients (160 implants). All patients had implants removed, thus allowing confirmation of the presence or absence of rupture. Clinical examination positively identified only one patient with implant rupture, and mammography detected only two implant ruptures (both extracapsular). The sensitivity for US was 70% and specificity was 90%, while for MRI it was 75.6% and 94%, respectively. These differences between MRI and US were not statistically significant. Combining the results of US and MRI did not seem to add to the diagnostic discrimination. The most cost-effective method of diagnosing implant rupture was US in our study.

Adult↗

Atypical chest pain syndrome in patients with breast implants.

Eleven patients, aged 36 to 55 years, with silicone breast implants had episodes of severe chest pain similar to heart attacks 6 weeks to 7 years after breast implantation; one patient had a severe attack 1 month after explantation. The chest pain, which was not related to physical exertion, lasted from 15 minutes to 4 days, and descriptions of it varied from a "pressing" type of pain to "stabbing" pain with radiation to the shoulders, left arm, and jaw. The associated symptoms were diaphoresis, nausea, vomiting, dyspnea, and palpitations. All of the patients had a normal electrocardiogram (ECG) with the exception of one, whose ECG showed nonspecific ST changes. Ten had cardiac evaluations, all of which yielded normal results. All had implant removal, and five were found to have at least one ruptured implant. Nine had an implant capsule biopsy; all had chronic inflammatory rinds, and five had free silicone in tissue whether or not the implants were ruptured. All eight who had a pectoralis major muscle biopsy had abnormal results: (neurogenic atrophy [six], fasciitis [three], myositis [one], chronic inflammation [one], free silicone [one], and neuroma [one]). We concluded that silicone breast implants may cause an atypical chest pain syndrome, probably due to local inflammatory reactions and neuroma formation.

Adult↗

Adjuvant breast disease: an evaluation of 100 symptomatic women with breast implants or silicone fluid injections.

We evaluated 100 referred women with breast implants (n = 97) or silicone fluid injections (n = 3) into breasts who developed various symptoms. All reported symptoms occurred at a median latency period of 6 years (range 0-24 years) after implantation or injection of silicone. Commonest symptoms were weakness (95%), fatigability (95%), myalgia (90%), morning stiffness (89%), arthralgia (81%), memory loss (81%), sensory loss (77%), headache (73%) and dry eyes and dry mouth (72%). Laboratory results revealed abnormal levels of serum immunoglobulins or complement in 57% and autoantibodies in 78%. Sural nerve biopsy was abnormal in 80% with the major finding of loss of myelinated fibers in 79%. Biceps muscle biopsy was abnormal in 58% with the major finding of neurogenic atrophy in 27%. Ninety-six patients underwent implant removal; 60% of the patients were found to have one or both implants ruptured with silicone spilled into tissue. At time of removal, a pectoralis major muscle biopsy was taken which was abnormal in 89% with the major finding of neurogenic atrophy in 55%. Biopsy of implant capsule was abnormal in 94% showing foreign body giant cells containing refractile material consistent with silicone in 69% whether or not the elastomer shell was ruptured. Silicone can cause a systemic autoimmune disease with a variety of symptoms probably due to a global activation of the immune system. Since our patients had objective laboratory and histologic findings together with a high rate of mechanical implant failure, further investigations are necessary.

Adult↗

IgG subclass deficiency in amyotrophic lateral sclerosis.

In order to get to clues about T-cell independent versus T-cell dependent immune mechanism in ALS, we measured IgG subclasses in 25 ALS-patients: 16 patients had deficiency of T-cell dependent expressed IgG1 or IgG3 or both with essentially normal levels of T-cell independent expressed IgG2 and IgG4. Ten of these patients had no prior treatment and five of these 10 had normal total IgG. Six patients had some immunosuppressive treatment before measurements of subclasses were done and all of them had deficiency of total IgG. Eight of 14 patients who underwent a d-xylose breath test, had evidence of small bowel overgrowth, which was confirmed by cultures of duodenal aspirate. IgG1 and IgG3 are T-cell dependent antibodies against protein antigens with close linkage on chromosome 14. The findings suggest a defect in the IgG subclass expression in ALS.

Adult↗

Structure and specificities of anti-ganglioside autoantibodies associated with motor neuropathies.

Autoantibodies that bind to GM1 ganglioside and asialo GM1 (GA1) have been implicated in the pathogenesis of motor neuropathies. To investigate the structure and specificity of these autoantibodies, peripheral blood B cells from patients with motor neuron diseases and from normal individuals were immortalized by EBV, and B cells secreting anti-GM1 or GA1 antibodies were cloned. We report an analysis of the structure and specificities of eight autoantibodies from patients with motor neuropathy, and two from normal individuals. Four antibodies were IgM, six were IgG, and all bound predominantly to GA1. The sequences of V domains of H and L chains were determined by a reverse transcription-polymerase chain reaction procedure. A variety of V genes were used to encode these antibodies: four VH1, two VH3, three VH4, one VH5, two V kappa I, two V kappa II, three V kappa III, and two V lambda II. Most V genes (13/19) exhibited less than 95% similarity to known germ-line genes, which suggests that somatic mutation was required to generate these autoantibodies, or that the relevant germ-line genes have not been identified. The average length of the H chain CDR3 was 16 amino acids, and in three antibodies this segment contained more than 20 amino acids. It was not possible to identify amino acid sequences that were encoded by germ-line D segments by conventional alignment of sequences. Partial analogies could be identified by introducing gaps, allowing mismatches and searching for D-D fusions and inversions. These results indicate that anti-GA1 antibodies can be encoded by a variety of VH-VL pairs, that the antibodies exhibit extensive somatic mutation, and that the CDR3 segments are generated by a number of nonconventional mechanisms.

Adult↗

The history of the neurological examination. Part 1: ancient and pre-modern history--3000 BC to AD 1850.

Every time a physician conducts a neurological examination the process continues a biomedical search for understanding the nervous system which is as ancient as the earliest civilizations in human history. Most of the modern neurological examination evolved in a short time span, between 1850 and 1914, but the origins of neurology as a medical quest for knowledge date to the first evolution of urban life, in the valleys of the Euphrates and the Nile. This paper reviews this history in two chronological segments: part 1 up to 1850 and part 2 the subsequent period.

History, Ancient↗

Lightning and electrical injuries.

Lightning and electrical injuries are similar in that both produce immediate tissue injury from burn and trauma induced by fall and both can arrest the heart and respiratory center. Immediate support of circulation and respiration is life-saving. Subsequently the nervous system may show signs of injury, and seizures, cerebral edema, and muscle and nerve lesions should be handled as the indications arise. Prevention of the injury is more effective than any postinjury treatment. Outdoors hikers and campers must take shelter to minimize their exposure; indoors properly installed equipment and attention to the relation of the equipment user to the electrical ground are the key elements in avoiding electrocution.

Electric Injuries↗

Neurology of microgravity and space travel.

Exposure to microgravity and space travel produce several neurologic changes, including SAS, ataxia, postural disturbances, perceptual illusions, neuromuscular weakness, and fatigue. Inflight SAS, perceptual illusions, and ocular changes are of more importance. After landing, however, ataxia, perceptual illusions, neuromuscular weakness, and fatigue play greater roles in astronaut health and readaptation to a terrestrial environment. Cardiovascular adjustments to microgravity, bone demineralization, and possible decompression sickness and excessive radiation exposure contribute further to medical problems of astronauts in space. A better understanding of the mechanisms by which microgravity adversely affects the nervous system and more effective treatments will provide healthier, happier, and longer stays in space on the space station Freedom and during the mission to Mars.

Adaptation, Physiological↗

Clinical correlations of anti-GM1 antibodies in amyotrophic lateral sclerosis and neuropathies.

Clinical correlations of antiganglioside GM1 antibodies are important because high titers of these antibodies may have therapeutic significance. To further evaluate this significance, we reviewed our experience with 78 patients who had the following diagnoses: amyotrophic lateral sclerosis (ALS), ALS syndromes in patients with gammopathy or thyroid abnormalities, cervical spondylosis simulating ALS, motor neuropathies, and chronic inflammatory demyelinating polyneuropathies (CIDP). Antiganglioside antibody titers were measured "blind" by ELISA assay at the neuromuscular clinical laboratory, Johns Hopkins School of Medicine. We conclude that anti-GM1 antibodies are found in a wide variety of neuromuscular conditions. Patients with classical ALS had a mean anti-GM1 antibody titer significantly lower than patients with CIDP or motor neuropathy. Patients with ALS associated with gammopathy or thyroid disorders had higher anti-GM1 titers than seen in classical ALS. The highest mean titer occurred in patients with CIDP, a treatable neuropathy.

Amyotrophic Lateral Sclerosis↗

The history of memory arts.

Ancient humans, lacking devices to store large amounts of information, invented and developed a system of mnemonics which evolved and passed to modern times. The mnemonics, collectively known as the Ancient Art of Memory, were discovered in 447 BC by a Greek poet, Simonides, and were adequately described by Cicero, Quintilian, and Pliny. These arts fell into neglect after Alaric sacked Rome in 410 AD, but were subsequently revived in 1323 by Saint Thomas Aquinas, who transferred them from a division of rhetoric to ethics and used them to recall Catholic doctrine and versions of biblical history. In 1540 Saint Ignatius Loyola used mnemonic images to affirm the faith with his newly formed Society of Jesus and tried to convert the Ming dynasty in China by teaching these memory skills to Chinese nobles. Today, the ancient memory arts have applications in pilot training, gambling, mentalism and telepathy demonstrations, and may have a role in the rehabilitation of brain-damaged patients. Objective testing confirms that with the use of these memory skills, recall is increased, at least 10-fold, and the memory deficits of proactive and retroactive inhibition do not exist.

History, 19th Century↗

Amyotrophic lateral sclerosis: abnormalities of the tongue on magnetic resonance imaging.

We compared the magnetic resonance images of the tongues of 16 amyotrophic lateral sclerosis (ALS) patients with those of 20 control patients and found the tongue in ALS patients is more frequently and more severely involved than suspected clinically, with major abnormalities of size, shape, position, and internal structure. The tongue size in ALS, as measured in the sagittal plane, can be reduced by as much as two-thirds of normal. The shape of the tongue in ALS tends to be rectangular or square rather than curved as is normal. As severity of the disease increases, the position of the tongue changes so that the bulk of the muscle falls away from the incisors and no longer is in contact with the hard or soft palate. The normal radial bands from the anterior floor of the mouth to the mucosal surface are often missing in ALS as are the two curvilinear bands that run parallel to the mucosal surface and intersect the radial bands. Also, there is a mottled disorganization of the internal structure of the tongue with areas of increased and decreased signal intensity.

Adolescent↗

Abnormal systemic metabolism of iron, porphyrin, and calcium in Fahr's syndrome.

Striopallidodentate calcinosis (Fahr's disease) is characterized clinically by seizures, rigidity, and dementia and pathologically by mineral deposition in the basal ganglia, dentate nucleus, and cerebral cortex. Disorders of iron and calcium-phosphate metabolism are thought to play a role in its pathogenesis. We present the case of a patient with familial striopallidodentate calcinosis who had porphyria cutanea tarda, refractory anemia, and pseudohypoparathyroidism type 2. The serum level of ferritin was markedly increased, serum iron and iron-binding capacity were below normal, and at autopsy she had deposition of iron in liver, spleen, bone marrow, and brain. She showed intermittent mild hypocalcemia, increased serum values of parathyroid hormone, elevated renal tubular reabsorption of phosphate, and low serum levels of 1,25-dihydroxyvitamin D, suggesting blunted renal responsiveness to endogenous parathyroid hormone. Pseudohypoparathyroidism type 2 was confirmed by infusion of synthetic parathyroid hormone, which gave a normal urinary cyclic adenosine monophosphate response, but a blunted phosphaturic response. After splenectomy for hypersplenism and weekly phlebotomies, she showed progressive improvement in function, mental status, weight, and seizure control. The hypothesis advanced is that the underlying pathophysiology of the separate diseases contributed to the formation of the brain stones through mechanisms of defective iron transport and free radical production.

Adult↗

Blepharospasm and autoimmune diseases.

We studied two patients, one with systemic lupus erythematosus and the other with myasthenia gravis, both of whom had coexistent blepharospasm. The blepharospasm occurred during exacerbations of the autoimmune diseases and improved with immunosuppressive therapy. These cases illustrate the possible association of blepharospasm and autoimmune disorders.

Adult↗