PubMed Health⌕ Search

Biomedical subjects

B L Annis

Publications and source records attributed to B L Annis.

6 recordsLinked to original sources
PubMed1996

Functional outcome after incomplete spinal cord injuries due to blunt injury.

During a 3-year period, 19 patients with incomplete spinal cord injuries caused by blunt trauma were admitted to a single rural referral centre. The mean age was 50 years. Injury mechanisms included falls in eight, road traffic accidents in five, diving mishaps in two, and miscellaneous in four. The level of spinal cord injury was cervical in 11, thoracic in five, and thoracolumbar in three. Initial management included a standard high-dose methylprednisolone protocol for 24 h after injury in eight patients treated since May, 1990. Neurosurgical procedures were performed in 11 patients. There were three deaths, all in patients over 75 years of age with pulmonary complications. Of 16 survivors, 10 demonstrated significant functional neurological improvement by the time of hospital discharge, and 11 by late follow up. Complete recovery occurred in five of the survivors. Complications occurred in 11 patients, including pulmonary (nine), infectious (six), and gastrointestinal (three), but could not be associated specifically with the high-dose steroid protocol. In conclusion, incomplete spinal cord injuries after blunt injury were relatively uncommon in this setting. No significant increase in complications was observed after institution of the high-dose methylprednisolone protocol in May, 1990. However, pulmonary, gastrointestinal, and infectious complications were common. Of the 16 survivors, 11 demonstrated significant functional improvement. Mortality appeared to be related to advanced age and to pulmonary complications.

Adolescent↗
PubMed1980

Recurrent Cushing's disease: successful treatment by pituitary irradiation or trans-sphenoidal hypophysectomy in two cases.

Two patients developed recurrent Cushing's disease 3 and 7 years after total bilateral adrenalectomy. In the first patient, a 65-year-old man, the adrenal tissue was not localized by radioactive cholesterol scintigraphy. Plain x-ray films of the skull revealed a normal sella turcica. Although clinical improvement resulted from the discontinuation of cortisone replacement therapy, urinary free cortisol levels remained elevated and the patient was treated with pituitary irradiation. Serum and urine cortisol levels gradually returned to normal. Four years after irradiation, the plasma adrenocorticotropic hormone (ACTH) concentration was elevated, but tomography of the sella turcica and urinary cortisol excretion remained normal. The second patient, a 41-year-old man, displayed elevated ACTH levels and x-ray evidence of a pituitary tumor at the time of recurrent Cushing's disease. After trans-sphenoidal hypophysectomy, the hypercortisolism abated and the ACTH concentration returned to normal. Adrenal scintigraphy frequently locates cortisol-secreting tissue in patients with recurrent Cushing's disease, and some investigators suggest treatment by the surgical removal of the adrenal remnant. Although the etiology of Cushing's disease is controversial, current evidence suggests that most cases result from ACTH-producing pituitary tumors. We suggest, therefore, that the anterior pituitary gland may be a more suitable target than the adrenal remnant for the treatment of recurrent Cushing's disease.

Adenoma↗
PubMed1978

Familial and acquired paroxysmal dyskinesias. A proposed classification with delineation of clinical features.

On a clinical basis the paroxysmal dyskinesias can be classified into two distinct categories--familial and acquired. The former begins in childhood and the dyskinesia may or may not be induced by sudden movements (kinesigenic or nonkinesigenic forms). In the familial kinesigenic form, the movements are brief, usually occur daily, and respond readily to anticonvulsants. This form has an autosomal dominant or recessive mode of inheritance. In the familial nonkinesigenic form, the movements are of longer duration, occur less frequently, and rarely respond to anticonvulsants. This form has a clear autosomal dominant mode of inheritance. The etiology is obscure. The acquired form of paroxysmal dyskinesia has a later onset and is an expression of an underlying neurological or metabolic disease. Some cases of acquired paroxysmal dyskinesia are manifestations of unusual forms of epilepsy. In these cases the differential diagnosis may be extremely difficult and must be based on EEG findings during an ictal episode.

Adolescent↗