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Biomedical subjects

L W Kneisley

Publications and source records attributed to L W Kneisley.

10 recordsLinked to original sources
PubMed1998

Medical and nondental treatments of snoring and sleep apnea syndrome.

The prevalence, pathophysiology, and clinical and polysomnographic evaluation of obstructive sleep apnea are reviewed. The history of the development of nasal continuous positive airway pressure, diagnostic titration of the treatment, abolition of nocturnal apneas, and consolidation of sleep architecture by nasal continuous positive airway pressure and long-term patient compliance with the treatment are discussed. The effects of weight gain and weight loss on the severity of obstructive sleep apnea, and cardiovascular and behavioral complications of obstructive sleep apnea are reviewed. Behavioral treatments are discussed.

Behavior Therapy↗
PubMed1990

Nocturnal stridor in olivopontocerebellar atrophy.

We describe a patient with olivopontocerebellar atrophy (OPCA) who was referred for alleged "snoring." Polysomnogram with video and audio monitoring revealed that the patient actually had nocturnal stridor causing repetitive oxygen desaturations. Direct laryngoscopy while awake showed a unilateral vocal cord paralysis. The nocturnal stridor persisted after unilateral vocal cord pinning, suggesting that the patient had probably been experiencing bilateral vocal cord paresis while asleep. We conclude that state-dependent vocal cord dysfunction may be severe in OPCA and related multiple system atrophy. Nocturnal stridor has many causes and may mimic snoring and obstructive sleep apnea syndrome. Polysomnography with audio and video recordings are necessary to make the diagnosis.

Arousal↗
PubMed1980

Paraplegia following surgery in Foix and Alajouanine syndrome. (Arteriovenous malformation of the spinal cord).

Two patients with spinal cord arteriovenous malformation became paraplegic after removal of the abnormal vessels from the dorsal surface of the thoracolumbar spinal cord. Surgical exposure of a spinal cord arteriovenous malformation without an attempt at removal accelerated the pace of progressive paraparesis in two other patients. The poor outcome of our cases is, however, not representative of modern surgical techniques, since selective spinal angiography and the operating microscope were not used. We propose that the intramedullary vascular changes in this condition are an integral component of the arteriovenous malformation. Additionally, the phenomenon of nocturnal seminal ejaculation in spite of progressing impotence may be a clinical feature unique to spinal cord arteriovenous malformations.

Adult↗
PubMed1978

Cervical spinal cord lesions disrupt the rhythm in human melatonin excretion.

To determine whether spinal cord lesions disrupt the diurnal activity of the human pineal, urinary melatonin levels were measured over 24 hours (4 or 8-hourly intervals) in male patients with clinical evidence of cervical spinal cord transection. During the waking state, levels of melatonin in these subjects ranged from 3.2--13.5 ng/4 hours; during sleep and darkness, values ranged from 1.8--10.5 ng/4 hours. Levels of serum cortisol, aldosterone, and growth hormone showed rhythmic variations in these subjects. The absence of significant nocturnal melatonin increases distinguishes quadriplegic subjects from normal males and from one subject with a lesion of the lumbar spinal cord. These differences may be caused by "decentralization" of the pineal organ due to a lesion within the cervical spinal cord interrupting descending sympathetic fibers. If so, the human pineal, like that of other mammals, is regulated, at least in part, by activity within the central nervous system via sympathetic nervous connections.

Adult↗
PubMed1977

Hyperhydrosis in paraplegia.

A 20-year-old man suffered head, chest, and abdominal trauma in an auto accident resulting in a traumatic dissecting aneurysm of the thoracic aorta. Hypotension developed. The aneurysm was resected and replaced with a prosthetic graft. Postoperatively, the patient was found to be paraplegic below T-9, areflexic and anesthetic to pain and temperature, with preservation of vibration and position senses. In the ensuing nine months, the patient regained considerable sensory function in his lower extremities and had severe constant hyperhydrosis below the T-9 dermatome. The exaggerated sweating was unaffected by temperature change and anxiety. It was diminished by methantheline bromide treatment but never abolished. The spinal cord lesion is postulated to be anterior horn cell loss, with preservation of interneurons and intermediolateral gray columns. Disinhibition of sympthetic circuits or sprouting of axons are proposed mechanisms.

Adult↗
PubMed1977

Delayed paralysis after cervical fracture-dislocation. Case report.

The authors describe the late development of ascending damage to the spinal cord after a cervicothoracic fracture-dislocation that produced no evidence of cord or nerve injury other than transient mild paresthesia in the arms. After 16 years, progressive quadriplegia developed with subsequent ascending dissociated sensory loss in the upper cervical dermatomes. The presence of a central syrinx was verified at operation 18 years after the injury.

Adult↗
PubMedDate not supplied

Treatable extramedullary cord compression. Meningioma as a cause of the Brown-Séquard syndrome.

The Brown-Séquard syndrome is infrequently reported. Though widely considered indicative of intramedullary spinal cord disease, in the absence of penetrating spinal cord trauma, the syndrome is frequently an early stage of extramedullary spinal cord compression, as an extensive analysis of diverse literatures reveals. We describe two cases resulting from compression of the spinal cord by a meningioma. While previous reviews emphasize that radicular or vertebral pain is a prominent feature of spinal cord compression by intradural tumors, our patients had no pain referable to tumor. Awareness that painless extramedullary spinal cord compression can produce the Brown-Séquard syndrome, early myelography, and surgical intervention are necessary to prevent progressive deficit. Even when encountered in a patient who has previously well-documented demyelinating disease, the syndrome should not be written off as a relatively untreatable intramedullary process.

Aged↗