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Four hundred and thirty-eight patients who had suffered a thromboembolic stroke not less than two weeks or more than four months previously, were entered into a placebo-controlled randomized clinical trial to determine whether suloctidil (200 mg t.i.d.) would influence the subsequent recurrence of stroke, the occurrence of myocardial infarction, or cardiovascular death. The two treatment groups were comparable at baseline with respect to important prognostic variables and there was good adherence to the study protocol during an average follow-up of 20 months. Significantly more patients complained of side-effects in the suloctidil group and more hepatotoxicity was also reported in the suloctidil group. Four cases of clinical hepatitis were suspected to be due to suloctidil, each of which was reversible on termination of study treatment; relative increases in SGOT and SGPT at three months in the suloctidil group were found to be mild and transient. The primary analysis of efficacy was based on the incidence of the first event of stroke, myocardial infarction or cardiovascular death, but excluding events that occurred more than 28 days after complete withdrawal from study medication for whatever reason. Thus, the primary analysis included 38 events in the suloctidil group and 47 in the placebo group (p = 0.17) representing a risk reduction of 24%. If total mortality is substituted for cardiovascular death, the corresponding figures are 47 in the suloctidil group and 58 in the placebo group (p = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Some time after deletion of occlusion of the appropriate artery, 20 patients had transient ischemic attacks and seven had strokes. The common statement that transient ischemic attacks cease when an artery becomes occluded must, therefore, be modified. Seventeen of the 20 patients reported here developed symptoms weeks to years after the appropriate artery was known to be occluded, while 10 attacks occurred within 1 week after occlusion. Embolism through collateral circulation probably accounts for the delayed ischemic events in most of the patients, and hemodynamic factors in a few. The stump of the occluded artery may be the site of atheromatous ulceration. The possibility of revascularization procedures for patients with occluded arteries makes pertinent these observations about potential embolic sources.

Five adults with primary intraventricular hemorrhage are described. The presenting features included headache, confusion and drowsiness. Focal neurological signs were minimal or absent. All five had a history of hypertension, three patients had bilateral internal carotid occlusion at its origin, one had unilateral occlusion of the left internal carotid artery with severe stenosis of the contralateral siphon. Unilateral occlusion of the middle cerebral artery were present in the fifth patient. Pathological examination of the brain from one patient showed the presence of severe hemorrhagic "lacunar" infarcts adjacent to the left lateral ventricle, one showing direct continuity of blood in the lacune with the massive intraventricular hematoma. We hypothesize that such a finding illustrates one possible mechanism for this unusual type of hemorrhage. Patients with longstanding hypertension and severe occlusive disease of the internal carotid arteries may be predisposed to this unusual complication.

Thrombi defined as intraluminal filling defects detected by angiography were identified in 30 patients (29 in the carotid system, one in the vertebral artery). Stroke was the presentation ipsilateral to the thrombus in 22 patients (12 had previous transient ischemic attacks), transient ischemic attacks occurred alone in seven cases, and one patient was asymptomatic. Angiography revealed a severe stenosis in association with the thrombus in 23 patients, a moderate stenosis in four patients, and, in the three patients with only minimal stenosis presumably due to atherosclerosis, there was evidence for a coagulopathy. Sixteen of the 30 patients were operated on urgently, 10 within 24 hours of detection of the thrombus. Twelve of these 16 surgical patients were given anticoagulation before surgery. At endarterectomy, thrombus was identified in 11 of the 14 surgical patients in whom the thrombus was accessible; the other two surgical patients had intracranial thrombus only. In this group, four of 11 surgical patients with accessible thrombi suffered perioperative episodes of new or larger infarction. Fourteen of the 30 patients initially received medical management with no complication. Eight of these 14 medical patients had repeat angiography; seven exhibited complete resolution of thrombus, and six of these seven patients subsequently underwent delayed endarterectomy for the stenosis. No thrombus was identified at surgery in any of the six. One of the six delayed surgery patients suffered a perioperative stroke. Although these numbers are small, reflecting the rarity of thrombus demonstrated by angiography, undetected thrombus is often found at endarterectomy. Its presence may increase operative risk.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors prospectively evaluated the clinical event rate over a 72 hour period following femorocerebral angiography in 1002 procedures. The neurologic event rate was 1.3 per cent in the first 24 hours (0.1% permanent) and 1.8 per cent between 24 and 72 hours (0.3% permanent). The non-neurologic event rate (mostly hematomas) was 7.2 per cent. There were no deaths. One hundred and nine pieces of data per procedure were analysed statistically. Delayed cerebral ischemia does occur and could be secondary to the procedure. The low risk of judiciously performed cerebral angiography was confirmed. Carefully cataloguing all events for up to 72 hours neither verifies nor excludes angiography as the cause of deterioration.

We studied 17 patients with atherosclerotic bilateral occlusion of vertebral arteries (VA) identified by angiography. Seven had vertebrobasilar TIAs, eight a brainstem stroke (severe in two), and two had only carotid symptoms. Brainstem strokes were more frequent with bilateral intracranial occlusion (60%) than with at least one extracranial occlusion (28.6%), but long-term prognosis did not differ in these two groups. In follow-up, the mortality rate was 4.5% per year, and the stroke rate was 1.8% per year. Major functional disability was seen in 16.7% of the survivors. Bilateral distal VA occlusion may sometimes have a better prognosis than previously assumed. These findings raise doubts about the value of extra-intracranial surgical bypass procedures in patients with these lesions.

It has been accepted that transient monocular blindness (TMB) is highly suggestive of an ipsilateral carotid artery lesion in patients with arterial risk factors. We confirmed this in 55 patients, who had an internal carotid artery severe stenosis, occlusion or ulceration on angiography in more than 50 per cent of the cases. However, 12-lead-ECG, 2 D--echocardiography and Holter monitoring also showed a potential cardiac source of emboli in 22 per cent of the patients. Most of these patients (83 per cent) also had an appropriate arterial lesion, and the exact cause of the episodes of TMB remained undetermined. Our study shows that every fourth of fifth patient with TMB may have a potential cardiac source of emboli, the detection of which could alter the management. Systematic non-invasive cardiac investigations are warranted, especially in TMB patients with known heart disease.

The advent of EC/IC Bypass surgery has focused attention on selected patients who might benefit from this innovative procedure. There is a poverty of natural history data pertaining to all such lesions. Two centres (Memphis, Tennessee and London, Ontario) pooled their resources to carry out a retrospective review of 58 patients with angiographically-proven intracranial internal carotid artery stenosis. Only 33% of the patients were alive and free from subsequent cerebral vascular events at the end of the mean follow-up of 30 months. Forty-three percent of the patients died during follow-up: 36% due to stroke and 44% because of cardiac disease. Forty-three percent of the patients suffered cerebral vascular events during the follow-up period: there were 17 strokes (29%) including 9 fatal strokes. The incidence of ipsilateral stroke was 19%; 65% of the strokes were appropriate to the stenotic intracranial carotid lesion under study. The annual ipsilateral stroke rate for patients with this lesion was 7.6% per year. This lesion detected on angiography is indicative of severe atheroma, and carries a serious risk of death due to ischemic heart disease or stroke.

In a retrospective study of 32 patients with "proven" syringomyelia and 15 patients with an alternate proven diagnosis, a change in the caliber of the spinal cord with different positions ("collapsing cord sign or cord collapse") had a sensitivity of 38% and a specificity of 87%. Central cord enhancement ("bull's-eye") on delayed CT had a sensitivity and specificity of 91% and 87%, respectively. The positive predictive value of cord collapse was 87%, while the positive predictive value of central cord enhancement was 94%.

To determine the value of extracranial-intracranial arterial anastomosis (EC/IC bypass), we randomly allocated 1377 patients with symptomatic atherosclerosis of the internal carotid or middle cerebral arteries to medical care alone or to EC/IC bypass with continuing medical care. As previously reported, surgery did not reduce--or significantly increase--the risk of stroke. Functional status data collected during the trial provide new information. Six weeks following entry, surgical patients showed greater dysfunction in the following activities: fluency of speech, getting in and out of bed, sitting down and standing up, toileting, cutting food and pouring beverages, and dressing and undressing. At 4.5 months, surgical patients still exhibited greater dysfunction in toileting, with nonsignificant trends in several other activities. From six months onward, there were no significant differences between the groups. Thus, EC/IC bypass results in transient worsening of functional status beyond the immediate perioperative period.

During a prospective trial of platelet-inhibiting drugs in patients with transient ischaemic attacks (T.I.A.s), 14 patients had serious neurological dysfunction and normal cerebral angiograms. The patients (mean age 37 years) had neurological episodes over a period of 1-4 years consisting of acute non-progressive strokes with residual symptoms. In 3 patients, the two cerebral hemispheres were involved on different occasions. Cerebral angiograms showed no significant atheromatous disease in the intracranial or extracranial vessels. 3 patients had mid-systolic clicks, 5 had systolic murmurs, and 2 patients had both a click and a murmur. Holter electrocardiographic monitoring revealed atrial, junctional, or ventricular extrasystoles (5 patients), paroxysmal atrial fibrillation (3), and paroxysmal ventricular tachycardia (1). Left ventricular angiography confirmed mitral-leaflet prolapse in all the patients. The focal nature of the T.I.A.s suggests an embolic event, the embolus arising from the abnormal mitral valve. In a patient not included in this series, a small antemortem left atrial thrombus was found at necropsy.

Eight cases of presumed acute occlusion of intracranial arteries, 7 middle cerebral and 1 posterior cerebral, demonstrated the occluded artery as an abnormal high density structure on non-enhanced computed tomography. Three cases underwent subsequent angiography which confirmed the diagnosis. CT scanning is therefore able to visualize acute thromboembolism in the intracranial arteries. In the appropriate clinical setting of acute stroke, an artery visualized on non-contrast CT scan as diffuse high density and higher in density than other visualized vessels should be suspected as acutely occluded by clot.

The clinical, pathological, and neurochemical characteristics of a newly recognized inherited neurological disorder are reported. Lethargy and mental depression are early symptoms, followed by mild parkinsonism and progressive weight loss. Failure of automatic respiratory control develops and may result in sudden death. Advanced degeneration of the substantia nigra, cell loss and gliosis of the basal ganglia, and focal gliosis in the medulla are seen on pathological study. Degeneration of the nigrostriatal dopaminergic system is evidenced by low levels of tyrosine hydroxylase, dopamine, homovanillic acid, and L-dopa decarboxylase in postmortem brain samples. Taurine concentrations in fasting plasma and CSF are somewhat depressed; brain contents of taurine are within normal limits.

A patient developed paraparesis and signs of meningeal irritation spontaneously while on anticoagulant therapy. At autopsy, a subdural hematoma of the thoracic cord and evidence of widespread subarachnoid hemorrhage were found. The possible mechanism for these combined hemorrhages is discussed.

A rapid electrometric method for determining endogenous and added CO 2 in fish products was studied using an Orion CO 2 probe and Orion ionalyzer model #801. Analytical results were compared to those using the standard Warburg manometric technique. Comparisons showed a ± 20.8% mean difference for low concentrations of CO 2 (<350 ppm) and a ± 10.7% mean difference for high concentrations of CO 2 (>800 ppm). The probe technique was found to be easier to use and required less time for operating and cleanup procedures than the manometric method. Based on recovery studies, the specific ion probe was more accurate at all levels of CO 2 evaluated than the manometric device.

A series of 9 patients have experienced hemisphere and retinal ischemia at an interval after occlusion of appropriate internal carotid arteries. All had radiological evidence of a persisting proximal stump to the occluded artery and, in most, pathological evidence of thrombotic material attached to atheromatous lesions within the stump. Thromboembolism from the stump via the anastomotic supply through ipsilateral common and external carotid arteries is thought to be responsible for the ischemic events to the brain or retina despite absence of flow through the internal carotid artery. Seven of the 9 were treated by surgical excision or obliteration of the stump and, when indicated, common and external carotid endarterectomy. Turbulence in the stump contributed to progressive atherosclerotic changes and probably aggravated thrombogenesis in this location with subsequent embolization into the anastomotic arteries.

Three hundred and fifty-two patients with atherosclerotic middle cerebral artery stenosis (MCAS, 53%) or occlusion (MCAO, 47%) have been systematically studied. The study involved all patients entered into the EC/IC Bypass Study with isolated MCA disease or a tandem lesion predominating in the MCA ipsilateral to the ischemic events (18 patients with a tandem lesion of greater magnitude in the internal carotid artery were not included). The Asian patients represented 58% of all Asians entered into the EC/IC Bypass Study, whereas the white patients represented 18% of all whites and the black patients 34% of all blacks. Isolated TIAs were less frequent in MCAO (12%) than in MCAS (34%). Warning TIAs before a stroke occurred in one third of the cases. Presentation with stroke or isolated TIA was not influenced by sex, age, level of MCA obstruction, collateral circulation nor associated carotid disease. In MCAS, no major difference in presentation was found between severe and moderate stenosis. Pure motor hemiparesis occurred in 15% and pure sensory stroke in 2% of the patients with stroke and 30% of the MCA territory infarcts were small and limited to the lenticulocapsular area, confirming that so-called lacunar infarcts may be due to large vessel disease. During follow-up (42 months) of 164 medically-treated patients, further cerebrovascular events (TIA and stroke) occurred in 11.7% of the patients per year. In MCAO the stroke rate was 10.1% per patient-year and the ipsilateral infarct rate was 7.1% per patient-year. In MCAS, the stroke rate was 9.5% per patient-year and the ipsilateral stroke rate was 7.8% per patient-year.(ABSTRACT TRUNCATED AT 250 WORDS)

A 46-year-old woman under investigation for three episodes of amaurosis fugax in the left eye proved to have a left anterior-middle fossa dural arteriovenous malformation with pial venous drainage. The malformation received its main supply from the left middle meningeal artery, but its anterior part was fed by the recurrent meningeal branch of the left ophthalmic artery. Transient episodic lowering of retinal arterial pressure due to shunting of blood from the ophthalmic artery to the malformation is the most likely explanation for the occurrence of amaurosis fugax, indicating that this symptom occurs in some patients on a hemodynamic basis.

The presenting characteristics of 74 patients with atherosclerotic occlusion of both internal carotid arteries are described. All had suffered either ischaemic hemisphere infarcts (80%) and/or transient ischaemic attacks (80%) involving one (78%) or both (22%) carotid territories. In addition, 10 subjects (14%) incurred recurrent vertebrobasilar or presyncopal episodes, many of which appeared secondary to haemodynamic insufficiency. The incidence of risk factors and concomitant vascular disease was high; 93% gave a history of heavy smoking. Thirty-four subjects were treated conservatively and followed prospectively for a mean of 42 months. Eighteen patients (53%) suffered further cerebrovascular events, an ischaemic event rate of 15% per patient per year. These were isolated transient ischaemic attacks (TIAs) in 7 and stroke in 11 patients. The latter suffered a total of 15 strokes during the follow-up period of 42 months; the annual stroke rate was 13% per patient year. Patients who had presented with ischaemic events involving more than one carotid territory were significantly more prone to subsequent cerebral infarction than those in whom symptoms had been confined to one territory (P less than 0.05). None of the 5 patients with haemodynamic TIAs who were managed conservatively developed a stroke during the follow-up period and their symptoms remitted spontaneously. Deaths per year amounted to 8%. Twenty-four patients (71%) survived, of whom half were either symptom-free or minimally disabled. In this group of preselected patients, which excludes those with severe deficits at presentation, bilateral occlusion of the carotid arteries may be a condition compatible with useful existence.

We evaluated 32 young patients with mitral valve prolapse (MVP) as the only recognized cause of cerebral ischemia. The mean follow-up from the time of the first ischemic event was 8 years. At the time of the follow-up evaluation, 24 patients (75%) had a normal cardiac examination, and 4 had midsystolic clicks; only 1 had the characteristic click-murmur. In 75%, the first ischemic event was stroke. When MVP-associated ischemia was recognized, 44% had recurrent ischemic events. In the mean 4-year period between diagnosis of MVP-associated ischemia and follow-up, 16% had recurrent ischemic events, but none had a new persistent deficit from these events. At the time of follow-up, 63% of patients were taking platelet antiaggregants or anticoagulants. These data suggest a good prognosis for recurrent ischemic events after diagnosis of MVP-associated ischemia.

Neurological, CT and high-field (1.5T) magnetic resonance imaging (MRI) data were correlated in 6 patients previously clinically diagnosed as having suffered small vertebrobasilar infarct. MRI demonstrated infarcts in areas where CT was nearly always negative. MRI allowed very precise clinico-topographic correlations and appears to be the preferred imaging technique in vertebrobasilar infarcts.

Bilateral occlusion of the middle cerebral artery (MCA) trunk theoretically should be a very severe condition, but its actual prognosis has never been studied. Nine of 1,377 patients (7 Asians, 1 Black, 1 Caucasian) from the Cooperative Study of Extracranial/Intracranial Arterial Anastomosis were found to have atherosclerotic bilateral occlusion of the middle cerebral artery (MCA) trunk before entering the trial. Three presented with a stroke followed by a contralateral stroke, two experienced a unilateral stroke, two had a unilateral stroke preceded by ipsilateral TIAs, one had a unilateral stroke preceded by TIAs on both sides and one experienced isolated unilateral TIAs. Retrograde filling to the distal MCA was universally present. During follow-up (mean: 45 months), only one (non-operated) patient had further cerebrovascular events, and ultimately a fatal stroke. One additional patient died of sepsis and one had a silent myocardial infarct. All survivors resumed their previous activities. This study shows that in bilateral MCA trunk occlusion, the long-term prognosis is reasonable in the patients who do not present with a devastating stroke.

Forty-seven patients with ICA occlusion and who presented either without any or only a mild neurological deficit were prospectively followed for an average of 34.4 months. During this period of time, 11 patients (23.5%) suffered a cerebral infarction of which two-thirds were ipsilateral to the occluded artery. The stroke rate distal to an occluded ICA artery was 5% per year. Twenty-four patients (51%) continued to experience TIA's in the territory of the occluded artery. The mortality rate was low (8.5%) during follow-up. Whether extracranial-intracranial bypass surgery will decrease the risk of cerebral infarction in this subgroup of patients is unknown. The International EC/IC Collaborative Trial may elucidate this point because this subgroup represents one of the randomization strata of that study.

Small infarctions of the medulla produce typical neurologic deficits and can be clinically recognized fairly reliably. High-field magnetic resonance imaging with a 1.5 T prototype scanner successfully demonstrated very tiny medulla infarctions in three of five patients. These lesions were imaged readily by a fairly rapid (approximately 1-2 min scan time) partial-saturation technique and confirmed on multiple spin-echo images. In addition, in two cases vertebral occlusion ipsilateral to the infarction was suggested by high signal on T2 weighted spin-echo images.

The natural history of MCA occlusion has become increasingly important since the surgical option of EC/IC bypass surgery has been available. The clinical course of 24 patients with angiographically-demonstrated occlusion of the MCA artery was reviewed. Eight patients presented with a major disabling stroke and five of these died during the acute phase of this ischemic event. The remaining 19 patients were followed for a mean of 54.2 months. There were five deaths in follow-up and two of these were due to subsequent strokes. Fourteen patients manifested a benign course: one of these had a further minor stroke and four had TIAs. Altogether, 3 strokes occurred during the follow-up period (2 fatal, 1 minor) and all were in the territory of the artery known to be occluded. Of those patients who survived their presenting ischemic event, 12 (63%) remained completely functional in terms of activities of daily living. MCA occlusion does not necessarily carry a poor prognosis with medial therapy alone and the role of bypass surgery hopefully will be clarified by the ongoing clinically randomized trial.

We assessed the value of clinical electrophysiologic study using intracardiac recording and programed electrical stimulation in 34 patients who had unexplained syncope and/or presyncope. All patients had normal electrocardiograms, and no abnormality was detected by clinical examination, ambulatory electrocardiographic recording, or treadmill testing. The electrophysiologic results were diagnostic in four patients (11.8 percent) and led to appropriate therapy that totally relieved symptoms. The results were abnormal but not diagnostic in two patients (5.8 percent) and normal in the remaining 28 patients (82.4 percent). The patients were followed for a mean period of 15 months (range two to 44) after electrophysiologic testing. Sixteen patients (47 percent) had no further episodes in the absence of any intervention. In four patients (11.8 percent), a definitive diagnosis was made during follow-up. In seven patients, permanent pacing was instituted empirically with relief of syncope. Two patients continued to have syncopal spells. We conclude that the diagnostic yield of electrophysiologic testing is low in a patient population that has no electrocardiographic abnormality or clinical evidence of cardiac disease. Empirical permanent pacing in patients with symptoms continuing after our study appeared to be beneficial, but this result is difficult to evaluate because of the high incidence of spontaneous remission in this group. Persistent attempts to document electrocardiographic abnormalities during a typical episode of symptoms appears to be the only definitive way to confirm or exclude an arrhythmic cause of the symptoms.

Two patients with osteopetrosis were studied in whom severe stenosis of one or both internal carotid arteries was demonstrated. One patient had autosomal dominant osteopetrosis and the other patient had the autosomal recessive form of the disease. In one patient, probable occlusion of one internal jugular vein and retrograde thrombosis of the contributing dural venous sinuses was present. Venous drainage of parts of the brain occurred through dilated emissary and scalp veins. It appears that major extracranial vessels may be impinged upon by dysplastic bone in osteopetrosis, although this is the first report of such an occurrence. A posterior fossa aneurysm was present in one case, and may have been related to abnormal intracranial hemodynamics.

A total of 1,377 patients with symptomatic obstructive cerebrovascular disease (most commonly, internal carotid artery occlusion) entered a trial in which they were randomized to either medical or surgical (extracranial-intracranial bypass) therapy. All but 8 had hemoglobin estimations performed at entry. The patients were followed for an average of 55.8 months. In the medical group, the 325 patients with high normal hemoglobin concentration (15 g/l or more) suffered no more ischemic strokes than the 382 patients with lower values (less than 15 g/l). Those strokes that did occur were no more severe in the high than the low hemoglobin group. Hemoglobin concentration did not emerge as a prognostic factor in those patients treated surgically (n = 662). This prospective study counters the hypothesis that high normal hemoglobin concentration is associated with poor outcome in patients with symptomatic obstructive disease of the carotid and cerebral arteries.

Three patients with focal brain-stem oculomotor disturbances (nuclear sixth nerve syndrome, sixth nerve palsy, bilateral internuclear ophthalmoplegia) as a consequence of multiple sclerosis have been studied with high-volume delayed computed tomography and high-field magnetic resonance imaging. In all of them, high-volume delayed computed tomography was inconclusive in the brain stem, but magnetic resonance imaging showed an area of prolonged T1 and/or T2 in the region appropriate to the oculomotor findings. Magnetic resonance imaging is the imaging technique of choice of small plaques in the brain stem. It can considerably aid clinicotopographic correlation in multiple sclerosis.

In the Canadian Cooperative Study of aspirin and sulfinpyrazone in patients with threatened stroke, there was no demonstrable benefit of sulfinpyrazone but there was a significant overall risk reduction in stroke or death of 31% with aspirin (p less than 0.05). This benefit of aspirin was restricted to males, in whom the risk reduction in stroke or death was 48% (p less than 0.005). As with a large-scale clinical trials, questions have been raised about the methodology of the study, including the type of patient included, the choice of outcome measures, the factorial design and the analysis of subgroups. In this report, the design and principal results of the study are summarized and the above methodologic concerns are discussed.

A double-blind, randomized, pilot trial of the calcium channel antagonist PY108-068 was completed in patients with acute ischemic cerebral infarction. Nine treated patients received PY108-068 orally (150 mg/day in divided doses) and 10 control patients received placebo within 48 hours of stroke onset for 21 days. The mean age of the treated patients (four men, five women) was 63.7 years and of the control patients (seven men, three women) 64.4 years. Most infarctions were in the territory of the middle cerebral artery. One treated patient died of sudden cardiac death on Day 12; one control patient died of cerebral herniation. Two treated patients had episodes of clinically insignificant hypotension during Day 1 of treatment. Two control patients had myocardial infarctions during the trial. The mean Toronto Stroke Scale scores at stroke onset were 67 and 90 and at Week 12 were 22.5 and 34.7 in the treated and control groups, respectively. There was parallel improvement in the two groups, with no significant difference between groups (p = 0.12). The mean Barthel Index functional scores at stroke onset were 32.8 and 33 and at Week 12 were 90 and 78.8 in the treated and control groups, respectively. There was a trend in favor of the treated group, but differences between groups did not reach significance. In this pilot trial, PY108-068 was found to be safe but not effective in patients with acute ischemic cerebral infarction.

Six cases of syringomyelia associated with intramedullary tumor were examined by metrizamide myelography and delayed computed tomography. All cases showed opacification of syringomyelic cavities 7-24 hr after myelography. This finding suggests that metrizamide can pass through the cord substance from the subarachnoid space into a syrinx cavity in noncommunicating types of syringomyelia. It supports the theory of transneural passage of fluid as part of the origin of such cavities. These cases also support the thesis that, in patients with cord cavities, tumor can be excluded only if the cavity is demonstrated within all areas of cord enlargement.