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Biomedical subjects

E F Wijdicks

Publications and source records attributed to E F Wijdicks.

At least 163 records · Page 9Linked to original sources
PubMed1990

Acute relapsing Guillain-Barré syndrome after long asymptomatic intervals.

Five patients who recovered from an initial episode of Guillain-Barré syndrome had acute relapses 4, 10, 15, 17, and 36 years later, respectively. Two patients had multiple subsequent relapses. The antecedent illnesses, distribution of weakness, and clinical courses of each relapse were similar for each patient, except that relapses in three patients were briefer than the initial episode. One patient had asymptomatic sarcoidosis. Pharyngeal, oculomotor, and diaphragmatic weakness requiring a ventilator were common. Complete recovery or mild residual deficits, return of reflexes, normal cerebrospinal fluid protein at the onset of recurrent episodes, and normal or virtually normal nerve conduction velocities at various times distinguished these patients from those with more typical chronic relapsing inflammatory polyneuropathy.

Acute Disease↗
PubMed1990

Blood pressure fluctuations in the dysautonomia of Guillain-Barré syndrome.

A 76-year-old man with severe Guillain-Barré syndrome had extremes of hypotension alternating with hypertension. His blood pressure paralleled both systemic vascular resistance and cardiac output. Heart rate, rather than stroke volume, was the major determinant of cardiac output over a wide range of blood pressures. It was at times invariant for several hours and was unresponsive to carotid massage or respiratory cycles, but slowed slightly with each episode of hypotension. Trend monitoring indicated that hypotension preceded reductions in pulmonary artery diastolic pressure. These findings suggest that hypotension resulted from a vasodepressor response with a vagotomized heart and that hypertension was the result of increased sympathetic activity. Both extremes were caused by parallel changes in vascular resistance and heart rate. Dysfunction of baroreflex buffering may have accounted for the rapid swings in pressure.

Aged↗
PubMed1990

Electrodiagnostic abnormalities in 113 consecutive patients with Guillain-Barré syndrome.

We performed electrodiagnostic tests on 113 consecutive patients with acute Guillain-Barré syndrome (103 within 3 weeks of onset). The most common motor conduction abnormalities were proximal conduction block alone (27%), proximal block associated with a distal lesion (27%), and generalized slowing (22%). Other combinations of abnormalities each occurred in fewer than 10% of patients. Thirty-seven percent of patients initially had normal sensory nerve conduction study results, most often in association with proximal conduction block. The characteristic early electrodiagnostic changes in Guillain-Barré syndrome were often present when cerebrospinal fluid protein concentration was still normal. Extensive early fibrillations occurred in 10 patients, 6 of whom recovered well. Patients with early generalized slowing of motor nerve conduction velocity, combined abnormalities, or low muscle action potential amplitudes in ulnar, median, and peroneal nerves generally, but not always, had poorer outcomes than patients with conduction block in one nerve segment. There was no consistent relationship between results of electrophysiologic studies and overall clinical grade or limb power, except that none of the patients with an isolated proximal block had virtual or complete paralysis in the same limb.

Adolescent↗
PubMed1990

Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage.

The association between hyponatremia and cerebral ischemia was investigated in a consecutive series of 208 patients with subarachnoid hemorrhage who had a daily fluid intake of at least 3 L and in whom fluid restriction, to correct hyponatremia, was not applied. Hyponatremia occurred in 70 (34%) of the 208 patients. The occurrence of cerebral ischemia in patients with hyponatremia, 17 (24%) of 70 patients, was significantly higher than in patients without hyponatremia, 17 (12%) of 138 patients (chi 2 = 4.028, p = 0.045). Cerebral ischemia was not more often fatal in hyponatremic patients than in patients without hyponatremia. We conclude that patients with hyponatremia are at increased risk of developing cerebral ischemia even if fluid restriction is not applied.

Brain Ischemia↗
PubMed1990

The effects of treating hypertension following aneurysmal subarachnoid hemorrhage.

We investigated in a consecutive series of 134 patients with aneurysmal subarachnoid hemorrhage whether institution of antihypertensive treatment was related to the incidence of cerebral ischemia and rebleeding. The aim of hypertensive treatment was to reduce the diastolic blood pressure to levels below 100 mm Hg. There was no difference in outcome between patients with or without antihypertensive drugs. Rebleeding was less frequent in patients with antihypertensive treatment (12/80 patients (15%) versus 18/54 patients (33%) without anti-hypertensive treatment (p = 0.012)). Nevertheless, patients with anti-hypertensive treatment had, on average, still higher blood pressures than untreated patients. Conversely, infarction occurred more often in patients with anti-hypertensive treatment (34/80 patients (43%) versus 12/54 (22%) without antihypertensives (p = 0.03)). This relationship was partly explained by co-existing hyponatremia. Our results suggest that the need for antihypertensive treatment is questionable, since the prevention of rebleeding is offset by an increased risk of cerebral infarction.

Antihypertensive Agents↗
PubMed1990

Outcome in perimesencephalic (nonaneurysmal) subarachnoid hemorrhage: a follow-up study in 37 patients.

We interviewed 37 patients with perimesencephalic hemorrhage, 18 months to 7 years after the bleed. None rebled or had persisting neurologic deficits. These findings are remarkably good compared with recent series of patients with subarachnoid hemorrhage and normal angiogram. When blood is confined to the mesencephalic cisterns in patients with normal angiogram, repeat angiography may not be indicated.

Adult↗
PubMed1990

De novo astrocytoma following immunosuppression in neurofibromatosis.

A 45-year-old man with a 20-year history of neurofibromatosis (NF-1) developed a massive astrocytoma 15 months following heart transplantation. CT before immunosuppressive therapy was normal. This is the 1st report of a de novo astrocytoma following immunosuppression in NF-1 and may indicate a causal relationship.

Astrocytoma↗
PubMed1989

Effect of fluid intake and antihypertensive treatment on cerebral ischemia after subarachnoid hemorrhage.

We prospectively studied 244 consecutive patients with subarachnoid hemorrhage who were admitted within 72 hours to the same institution between November 1977 and May 1987 and who were not treated with antifibrinolytics. From November 1977 through December 1982 (the first study period), daily fluid intake was 1.5-2.1 and fluid restriction was applied when hyponatremia developed; antihypertensives were administered to all patients with high blood pressure. From January 1983 through April 1987 (the second study period), daily fluid intake was at least 3 l, fluid restriction was not applied, and antihypertensives were administered only when patients were receiving this treatment before admission; calcium antagonists were not administered. Entry variables of the patients admitted during the two study periods were not significantly different, although patients admitted during the second study period were at slightly increased risks of developing cerebral ischemia and of having a poor outcome. Despite this, cerebral ischemia occurred less frequently among patients admitted during the second study period than among those admitted during the first (16 [10%] of 155 patients vs. 19 [21%] of 89 patients; p = 0.030). Overall mortality decreased from 46% to 36% while mortality among patients with cerebral ischemia decreased from 60% to 31% (difference not significant). Rebleeding and acute hydrocephalus occurred with the same frequency among patients admitted during both study periods. We conclude that the combination of increased fluid intake and the avoidance of antihypertensives helps prevent cerebral ischemia after subarachnoid hemorrhage.

Antihypertensive Agents↗
PubMed1989

Short-term tranexamic acid treatment in aneurysmal subarachnoid hemorrhage.

Antifibrinolytic treatment for 4 weeks after a subarachnoid hemorrhage has been shown to have no effect on outcome since a reduction in the rate of rebleeding was offset by an increase in ischemic events. To determine if a shorter course (4 days) of antifibrinolytic treatment before the expected onset of ischemic complications might reduce the rate of rebleeding yet avoid ischemic complications, we prospectively studied a series of 119 patients with subarachnoid hemorrhage; 479 patients with subarachnoid hemorrhage from our previous randomized double-blind study (238 treated with placebo, 241 with long-term tranexamic acid) served as historical control groups. At 3 months' follow-up, the outcome of patients treated with short-term tranexamic acid was not different from that of patients treated with long-term tranexamic acid. The rate of rebleeding (24 of 119, 20%) was near that with placebo (56 of 238, 24%). In contrast, the rate of cerebral infarction (33 of 119, 28%) was almost identical to that after long-term tranexamic acid (59 of 241, 24%), although mortality from cerebral infarction was reduced. Compared with historical control groups, treatment with tranexamic acid for 4 days fails to reduce the incidence of rebleeding but still increases the rate of cerebral infarction.

Cerebral Angiography↗
PubMed1989

Management problems in acute hydrocephalus after subarachnoid hemorrhage.

In a consecutive series of 473 patients admitted within 72 hours after a subarachnoid hemorrhage, 91 (19%) had hydrocephalus on the initial computed tomogram. Consciousness was unimpaired in 25 of the 91 (28%). In 11 more patients acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. Thirty-eight (8%) of all 473 patients subsequently showed clinical deterioration because of acute hydrocephalus; 11 of these 38 had fluctuations in the level of consciousness. Of the 66 patients with acute hydrocephalus and impaired consciousness on admission, 26 (39%) spontaneously improved within 24 hours. Ventricular drainage was performed in 32 (31%) of the 102 patients with acute hydrocephalus (7% of all 473 patients). Consciousness improved after ventricular drainage in 25 (78%) of the 32 patients. Ventriculitis developed in 12 of the 24 patients with external drainage, mainly after greater than 3 days of drainage, and in none of the eight patients with an internal shunt. Among the 340 patients with aneurysmal subarachnoid hemorrhage and no long-term tranexamic acid treatment, the frequency of rebleeding in patients with ventricular drainage (43% of 23) was significantly higher than in hydrocephalic patients without drainage (15% of 52 patients; chi 2 = 5.009, p = 0.025) and patients without acute hydrocephalus (20% of 265 patients; chi 2 = 5.521, p = 0.019). We conclude that spontaneous improvement occurs in half of the patients with acute hydrocephalus and impaired consciousness on admission, which is usually apparent within 24 hours, and that the outcome of patients who need ventricular drainage will improve if rebleeding and infection after insertion of the ventricular drain can be prevented.

Acute Disease↗
PubMed1989

Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage.

In this study with randomized controls, we administered fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion. Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days (from 63% to 38%, p = 0.041). A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days (p = 0.014) and during the entire 12-day study period (p = 0.004). Although fludrocortisone treatment tended to diminish the decrease in plasma volume, the difference was not significant (p = 0.188). More patients in the control group developed cerebral ischemia (31% vs. 22%) and, consequently, more control patients were treated with plasma volume expanders (24% vs. 15%), which may have masked the effects of fludrocortisone on plasma volume. Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Clinical Trials as Topic↗
PubMed1989

Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage.

We prospectively studied serial electrocardiograms in 61 patients with aneurysmal subarachnoid hemorrhage. Electrocardiographic changes were related to the initial level of consciousness, to subsequent events, and to outcome after 3 months. All 61 patients had at least one abnormal electrocardiogram, but cardiac disease did not contribute directly to morbidity or mortality. Fast rhythm disturbances, ischemic changes, or both on the electrocardiograms were significantly correlated with poor outcome but not with specific outcome events, particularly not with rebleeding or cerebral ischemia. The Glasgow Coma Scale score on admission and the amount of cisternal and (to a lesser extent) intraventricular blood on the initial computed tomogram were also significantly correlated with poor outcome, but these factors only partially confounded the relation between electrocardiographic abnormalities and poor outcome. We conclude that in patients with aneurysmal subarachnoid hemorrhage, electrocardiographic abnormalities do not herald impending cardiac disease but indirectly reflect adverse intracranial factors. Electrocardiographic abnormalities may therefore have some independent value in predicting poor outcome.

Arrhythmias, Cardiac↗