Magnetic resonance imaging measurements and clinical changes accompanying transtentorial and foramen magnum brain herniation.
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Brain Stem↗
Biomedical subjects
A H Ropper
Publications and source records attributed to A H Ropper.
Successful management of paraprotein-associated peripheral polyneuropathies by immunoadsorption of plasma with staphylococcal protein A.
Two patients with paraprotein-associated peripheral polyneuropathy were treated successfully using immunoadsorption of patient's plasma with staphylococcal protein A. Both had previously been treated with immunosuppressive agents or plasma exchange, and were rapidly relapsing at the time of their protein A immunoadsorption therapy. One patient was treated "on-line" with a blood cell separator, and one was treated "off-line." Both responded well to therapy with minimal toxicity. Serum levels of circulating immune complexes were elevated in one patient and remained so during and after therapy. Immunoadsorption with protein A should be investigated as a therapeutic option for patients with paraprotein-associated peripheral polyneuropathy. The therapy is relatively easy to administer, particularly "off-line," and was well tolerated by our patients. More experience, including formal clinical trials, will be required to properly define the indications for, and mechanism of response to, this therapy.
Aged↗
Acute respiratory failure neuropathy: a variant of critical illness polyneuropathy.
OBJECTIVE: To describe a severe axonal polyneuropathy that follows acute respiratory failure and, in turn, causes continued ventilator dependence and paralysis after resolution of the primary illness. DESIGN: Retrospective chart review of three patients and prospective analysis of two patients. SETTING: Respiratory and neurologic ICUs of a general hospital. PATIENTS: Five critically ill patients after an episode of acute respiratory failure. Neuromuscular blocking drugs were used in four patients, intermittently in two patients, high doses of corticosteroids were briefly administered in four, four patients had multiple organ failure, three patients had sepsis, but weakness preceded these complications in two patients. INTERVENTIONS: None. MAIN RESULTS: All patients had moderate-to-severe limb weakness with reduced or absent reflexes. Sensation was relatively preserved and the spinal fluid protein concentrations were normal. Electrophysiologic studies showed a severe, acute axonal motor neuropathy in four patients and normal studies in the fifth that later demonstrated denervation. Sensory potentials were mildly or not affected. Two quadriparetic patients died at 2.5 months, one remained weak and ventilator dependent several months after onset, and two patients recovered to walk in 4 to 6 months. CONCLUSIONS: Severe axonal motor neuropathy after acute respiratory failure probably represents a variant of "critical illness polyneuropathy" that can be recognized from the temporal course of a conversion from primarily pulmonary to a pattern of neuromuscular ventilatory failure.
Action Potentials↗
Syndrome of transtentorial herniation: is vertical displacement necessary?
MRI from a comatose patient with a massive acute subdural haematoma showed most of the features of transtentorial herniation described in the classic pathology literature. In addition to encroachment on the perimesencephalic cisterns, infarction in the anterior and posterior cerebral artery territories, ischaemic change in the lower diencephalon, and ventricular enlargement were visualised. Despite the clinical syndrome and these secondary changes due to compression, there was only approximately 2 mm of downward displacement of the upper brainstem compared with 13 mm horizontal displacement. Although tissue shifts adjacent to the tentorial aperture cause brainstem and vascular compression, these changes may occur with minimal downward herniation.
Aged↗
Human immune globulin infusion in Guillain-Barré syndrome: worsening during and after treatment.
Because of an unexpectedly high rate of worsening, we report the results of treatment of Guillain-Barré syndrome with a standard regimen of human immune globulin (HIG) in 15 consecutive patients. Patients were treated with 1.5 g/kg HIG for 4 days beginning a mean of 7 days after the first symptoms. Eight stabilized or improved, but seven deteriorated during or within the first 5 days after treatment, and four remained ventilator-dependent for at least 2.5 months. One had a severe relapse 5 weeks after treatment. Five patients subsequently received plasma exchange and two improved. Our experience varies from previous reports that have endorsed HIG treatment for Guillain-Barré syndrome.
Action Potentials↗
Seronegative, non-neoplastic acute cerebellar degeneration.
Five women are presented with a subacute pure pancerebellar syndrome of ataxia and dysarthria to emphasize that this illness may occur without anti-Purkinje-cell or anti-Yo antibodies, or associated systemic cancer. The syndrome evolved over weeks or less and stabilized in four of the patients. Three had had a preceding infection and one, a rash, but there was no inflammatory response in the spinal fluid. Over the 5-year period during which these patients appeared in an individual general neurology practice, there was only one patient with paraneoplastic cerebellar degeneration. Despite the association of this syndrome with cancer, particularly in women, clinicians will still commonly confront the idiopathic variety.
Adult↗
Early Guillain-Barré syndrome without inflammation.
A patient with typical acute Guillain-Barré syndrome died 72 hours after his first symptoms occurred, and an autopsy was performed 8 hours after his death. Extensive sampling of cranial and peripheral nerves, sensory ganglia, and autonomic nerves showed only minimal inflammatory lymphocytic and macrophage infiltrates. This case, one of the earliest studied extensively, represents an extreme example of a noninflammatory mechanism that has been proposed in some cases of Gullain-Barré syndrome.
Cranial Nerve Diseases↗
Acute intracranial lesions and respiratory sinus arrhythmia.
We studied the effects of acute intracranial lesions on the respiratory sinus arrhythmia (RSA) with the use of computerized measurements of the ratio of expiratory to inspiratory R-R intervals. The RSA was reduced below the 95th percentile for age in 20 of 27 patients, an average of 2 days after an acute event. Only four patients, without neurological deficits, had a normal RSA. Two patients, with signs of secondary brain-stem compression from a mass, had an increased RSA, without the bradycardia that is usually associated with Cushing's response. Twenty-three patients had their respiratory rate controlled by positive pressure ventilation during testing, and our preliminary findings suggested that this was not responsible for reducing the RSA. Acute intracranial lesions caused a diminished RSA, perhaps by reducing supratentorial influences on vagal cardioinhibitory activity. In contrast, once signs of secondary brain-stem compression occur, the RSA is greatly increased while the heart rate remains unchanged, offering a possible method of noninvasive monitoring for this complication.
Acute Disease↗
The brain stem viewed in situ from above.
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Brain Stem↗
Neurological intensive care.
Neurological intensive care has evolved from the principles of respiratory care established during the poliomyelitis epidemics into a broad field encompassing all of the acute and serious aspects of neurological disease. The economic and political complexities of modern intensive care play a major role in organizing a unit and building a program. Central themes of practice in modern neurological intensive care units include the clinical physiology of intracranial pressure, cerebral blood flow, and brain electrical activity; the systemic abnormalities and medical complications of nervous system diseases; postoperative care; and management of neuromuscular respiratory failure. Treatment of severe stroke and cerebral hemorrhage, brain death, ethical dilemmas of severe neurological illnesses, and the neurological features of critically ill medical patients are also becoming neurological intensive care pursuits. The "neuro-intensivist" is trained to defragment medical care by combining knowledge of neurological diseases with the techniques of intensive care. Future directions include the clinical implementation of brain resuscitation and brain-sparing therapies, sophisticated monitoring of electrophysiological and intracranial physiological indices, and further understanding of the dysfunction of other organs that follows brain and nerve failure.
Forecasting↗
A note on impotence in Guillain-Barré syndrome.
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Adult↗
Motor nerve inexcitability in Guillain-Barré syndrome. The spectrum of distal conduction block and axonal degeneration.
We studied 34 patients with the Guillain-Barré syndrome (GBS) to clarify the clinical significance of inexcitable motor nerves and of low amplitude compound muscle action potentials (CMAPs). The patients were subdivided into two groups. Group 1 included eight patients who had electrically inexcitable motor nerves within 2 wks of the first symptom. (Two patients without extensive conduction studies had only one inexcitable motor nerve.) The outcome in this group at 1 yr varied from complete recovery (five patients) to severe motor sequelae (three patients). Group 2 included 26 patients who had two electrophysiological assessments, and in whom the serial changes in CMAP amplitudes were analysed and correlated to outcome. Fourteen of these 26 sets of serial studies were performed within 1 mth. Twelve of 26 patients in Group 2 showed decrease in the amplitude of CMAPs between serial studies; only six of these had a good outcome at 1 yr. Nine of 26 patients showed increase in CMAP amplitude between serial studies, of these eight had a good clinical outcome. Low-amplitude CMAPs or inexcitable motor nerves in the initial stages of GBS are due to distal pathology of the motor axons, either distal conduction block or axonal degeneration. The nature of these changes cannot be predicted by the results of the initial electrophysiological evaluation, including the presence or absence of active denervation. However, improvement of CMAP amplitude on sequential studies suggests a good outcome at 1 yr. We believe that, in the absence of a biological marker for GBS, individualization of an 'axonal variant' of the syndrome is not warranted at the present time.
Action Potentials↗
Vasodepressor carotid sinus syncope associated with a neck mass.
We present the hemodynamic and autonomic features of recurrent purely vasodepressor syncope episodes in a patient with left-sided malignant cervical adenopathy involving the carotid sinus. Extreme hypotension lasting 10 to 30 minutes, without change in heart rate, occurred spontaneously and 20 seconds after head-turning. The baseline respiratory sinus arrhythmia, heart rate response to standing and Valsalva's maneuver, and cold-induced blood pressure elevation were normal, indicating normal baroreceptor function between episodes. The episodes abated after 1 week of bedrest but reappeared within 1 day of discharge from the hospital. Syncope no longer occurred after intracranial section of the left glossopharyngeal nerve and upper rootlets of the left vagus. Autonomic testing remained normal postoperatively. A review of the literature indicates that purely vasodepressor syncope has been more common with left carotid sinus lesions.
Blood Pressure↗
Serologic evidence of Campylobacter jejuni/coli enteritis in patients with Guillain-Barré syndrome.
We performed serologic testing for Campylobacter jejuni in 17 consecutive patients with acute Guillain-Barré syndrome from the Boston, Mass area to compare the frequency of this preceding infection with the high rates reported from other areas of the world. The rate of seropositivity, 18%, was considerable, but it was lower than that reported in Australia. Moreover, all of our patients with definite serologic evidence of infection had severe enteritis before Guillain-Barré syndrome, usually with the organism cultured from stool samples. Campylobacter enteritis is an important antecedent illness for Guillain-Barré syndrome but did not precipitate the disease without enteritis.
Antibodies, Bacterial↗
Clinicopathologic correlation in a case of pupillary dilation from cerebral hemorrhage.
A patient who developed pupillary dilation on the side of a large cerebral hemorrhage underwent serial examinations, computed tomography, and magnetic resonance imaging. Autopsy dissection was performed to allow in situ examination of the structures near the third nerves and tentorial edge. The origin of the oculomotor nerve was displaced medially, causing the distal nerve to "kink" over the clivus just posterior to the clinoid. Transtentorial herniation of the medial temporal lobe did not appear to play a role in third-nerve compression.
Aged↗
Ischemic compression paresthesias in Guillain-Barré syndrome.
An experiment in nine patients tested the similarities and interactions between the paresthesias of Guillain-Barré syndrome (GBS) and tourniquet-induced compression paresthesias. During brachial compression, GBS paresthesias diminished in five of seven patients and new paresthesias occurred in two patients with purely motor GBS. Beginning 1 to 4 minutes after release of the cuff, all patients had new paresthesias, distinguishable from GBS symptoms. The novel finding was that GBS paresthesias diminished or ceased during the postcompression period in five of seven patients. Demyelinated peripheral nerves in GBS apparently can generate and transmit the spontaneous activity associated with paresthesias in the postcompression period. Interference occurs between the two types of paresthesias, possibly because both are caused by spontaneous ectopic activity in tactile nerves.
Foot↗
Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study.
To identify those factors associated with cerebral hemorrhage among brains with cerebral amyloid angiopathy (CAA), we undertook a comparative postmortem histopathological study of amyloid-containing vessels in the brains of patients with and without hemorrhage. Those without hemorrhage were represented by the following two groups: (1) elderly patients from a large general hospital (n = 66; age range, 75-107 years) and (2) patients with various neuropsychiatric disorders (n = 70; age range, 27-96 years). CAA was found in 45% of the first group and in 54% of the second group. The findings in these patients were compared with those in 17 brains in which both CAA and cerebral hemorrhage were present. We found that CAA was more severe in the brains with cerebral hemorrhage than in those without, and that fibrinoid necrosis was seen only in the brains with cerebral hemorrhage (12 of the 17 brains). Microaneurysms occurred only in the presence of severe, rather than moderate or mild, CAA. Serial sections in 2 brains of patients with cerebral hemorrhage showed fibrinoid necrosis, microaneurysms, and vascular rupture in close association with the hemorrhage. In 2 patients, hemorrhage was precipitated by trauma, and in 1, it was secondary to metastatic carcinoma. The features of brains from patients with CAA that are most consistently related to cerebral hemorrhage are (1) a severe degree of CAA and (2) the presence of fibrinoid necrosis, with or without microaneurysms.
Adult↗