Search PubMed⌕ Search

Biomedical subjects

A H Ropper

Publications and source records attributed to A H Ropper.

At least 91 records · Page 5Linked to original sources
PubMed1986

Relapsing central and peripheral demyelinating diseases. Unusual pathologic features.

We treated a patient who had a demyelinating peripheral neuropathy and a central nervous system inflammatory demyelinating disease. The unusual pathologic feature of dense infiltrates of atypical macrophages was observed in many areas of the brain; otherwise the process had several features in common with either multiple sclerosis or chronic relapsing experimental allergic encephalomyelitis. The illness followed "swine-flu" inoculation; exacerbation followed pneumococcal vaccination.

Bacterial Vaccines↗
PubMed1986

Unusual clinical variants and signs in Guillain-Barré syndrome.

Limited regional forms of the Guillain-Barré syndrome (GBS) and unusual focal signs or symptoms that resemble other illnesses are described: pharyngeal-cervical-brachial weakness with ptosis, sparing power, and reflexes in the legs; paraparesis with normal power and reflexes in the arms; early severe ptosis without other signs of oculomotor weakness; and acute severe midline back pain at the onset. The first two variants did not progress to typical generalized GBS, delaying the proper diagnosis. Regional and functional variants suggest that the pathologic, and perhaps immunologic abnormalities of GBS can be localized and selective.

Adult↗
PubMed1986

Severe acute Guillain-Barré syndrome.

Six of 58 consecutive patients with Guillain-Barré syndrome had an acute, severe, and prolonged initial illness, with quadriplegia in 2 to 5 days and mechanical ventilation for over 2 months. The average times in the ICU, on a ventilator, in the hospital, and in rehabilitation were 62, 141, 157, and 148 days, respectively. Four were still bedbound and ventilated at 6 months. Three (5%) were limited to a chair, and three walked unsteadily or required foot splints 2 to 3 years after onset. Only 2 of 13 other ventilated patients with slower initial progression of weakness, and none of 38 nonventilated patients were chairbound 6 months after onset (1 died at 2 months); all were walking independently by a year. Quadriplegia appearing over 2 to 5 days is associated with the most severe and prolonged weakness and, in some patients, leads to a permanent chairbound state. Improvement stops at 1 1/2 to 2 years.

Acute Disease↗
PubMed1986

Evoked potentials in Guillain-Barré syndrome.

We studied evoked potentials (EPs) in 27 patients with typical acute Guillain-Barré syndrome and 3 with Fisher's syndrome. Three of 21 had BAEP abnormalities: 1 with bilateral I-III, 1 with unilateral I-III, and another with unilateral III-V interwave latency prolongations. Three with Fisher's syndrome had normal BAEPs (one had a poorly formed wave V unilaterally with one click polarity only). Ten of 21 median nerve EPs and 9 of 12 peroneal or tibial nerve somatosensory EPs were abnormal. Seven patients with normal somatosensory EPs had abnormal F waves from the same nerve; none had normal late responses and abnormal somatosensory EPs. These observations differ from previous reports on the frequency and interpretation of EP abnormalities in Guillain-Barré syndrome.

Adult↗
PubMed1985

Acute traumatic midbrain hemorrhage.

A syndrome resulting from traumatic midbrain hemorrhage is described in 5 patients, 3 of whom had intracranial pressure measurements and 2 of whom had pathological examinations. The major clinical signs, evident immediately after injury, are coma, dilated (4 to 8 mm diameter) pupils that are fixed to light and dark, diminished limb tone, and impaired horizontal eye movements. The hemorrhages are single and linear or oval-shaped in the midsagittal rostral midbrain, extending several millimeters bilaterally. The appearance of the hematoma may be delayed on computed tomographic scanning, but early abnormalities of wave V of the brainstem auditory evoked potentials aid in diagnosis. Pathological features suggest that secondary brainstem distortion occurred soon after injury, perhaps resulting from a transiently raised intracranial pressure, but shearing injuries caused by acceleration-deceleration forces were also found.

Accidents, Traffic↗
PubMed1985

Guillain-Barré syndrome: management of respiratory failure.

Nineteen of 38 consecutive patients with Guillain-Barré syndrome were treated with mechanical ventilation in a neurological ICU. A ventilator was used for expiratory vital capacity (VC) below 12 to 15 ml/kg or arterial PO2 below 70 mm Hg, or clinical signs of fatigue. Artificial ventilation was discontinued when VC reached 8 to 10 ml/kg. Twelve patients required tracheostomy at 11 days (mean) after intubation. Mechanical ventilation was required for 49 days (mean). Complications included pneumonia in 15 patients, mostly aspiration, only 1 severe; pulmonary embolus in 1 ventilated and 1 nonventilated patient; and tracheal stenosis in 1. There was one death in a previously unintubated patient who developed sepsis while improving from GBS, and no deaths in the 18 other intubated patients.

Adult↗
PubMed1985

Terminal electrocardiographic changes in brain-dead patients.

We analyzed ECGs of 18 brain-dead patients from the time of termination of ventilation until cessation of electrocardiographic activity. Gradual slowing of the atrial mechanism was followed by AV block or a gradually slowing junctional escape rhythm. Despite progressive failure of atrial and junctional pacemakers, none had a ventricular escape rhythm. There were three terminal rhythms: (1) atrial activity only, (2) slow junctional rhythm or sinus bradycardia, or (3) ventricular tachycardia (VT). A prolonged QT interval, corrected for rate, was related to later development of VT. One hypothermic and three euthermic patients had J waves.

Brain Death↗
PubMed1984

Brain edema after stroke. Clinical syndrome and intracranial pressure.

We studied prospectively the syndrome of brain edema after a large infarction in 12 patients. The major symptom was drowsiness, which began on the first to fourth day after the ictus and which was accompanied by asymmetry in pupillary size of 0.5 to 2.0 mm in eight patients, periodic breathing in seven, and Babinski's sign contralateral to the hemiparesis in five. These accompanying signs appeared several hours after drowsiness in some patients. Seven patients had brain death, one died of sepsis after recovering from brain swelling, and only four survived. In six patients in whom intracranial pressure was continuously measured, levels persistently above 15 mm Hg were associated with eventual brain death (four patients) and levels below 15 mm Hg were associated with survival (two patients).

Adult↗
PubMed1984

Mechanism of pseudotumor in Guillain-Barré syndrome.

A patient with pseudotumor cerebri and Guillain-Barré syndrome was studied with serial measurements of pressure-volume index, CSF outflow resistance (Ro), and CSF production rate. The results were comparable to findings in previous cases of idiopathic pseudotumor. Although Ro was elevated and progressively diminished as the pseudotumor syndrome improved, the extent of elevation in Ro was inadequate to account for raised CSF pressure. These results suggest an alternative explanation for pseudotumor based on raised effective venous pressures at points of CSF outflow that are passively reflected in raised CSF pressure. A parallel rise in vascular and CSF pressure may also explain why patients with pseudotumor tolerate such high intracranial pressures.

Adult↗
PubMed1984

Pain in Guillain-Barré syndrome.

The clinical features of pain were prospectively analyzed in 29 consecutive patients with Guillain-Barré syndrome (GBS). Sixteen (55%) had characteristic pain early in the illness described as similar to the muscular discomfort following exercise ("charley horse"). Pain preceded weakness by one to five days in four patients. The anterior and posterior aspects of the thighs, the buttocks, and the low part of the back were most frequently affected. Pain was frequently worse at night. Specific clinical signs or electrophysiologic abnormalities were not associated with pain, but serum creatine kinase level was elevated in ten of 13 patients with pain and only one of eight without pain. A review of previously reported pathologic material in five patients with GBS failed to disclose a relation between inflammation of dorsal root ganglia and pain. These results suggest that alterations in muscle related to neurogenic changes may cause the typical pain of GBS.

Creatine Kinase↗