Cerebral arterial air embolism after computed tomography-guided hook-wire localization of a pulmonary nodule: A case report.

RATIONALE: Cranial arterial air embolism is a rare but potentially fatal complication after computed tomography (CT)-guided pulmonary interventions. PATIENT CONCERNS: A 64-year-old man was diagnosed with a pulmonary nodule (diameter: approximately 1 cm) in the right lower lobe. The patient developed convulsions after CT-guided hook-wire localization. DIAGNOSIS: Cranial CT revealed arborizing/linearly distributed gas in the territory of the right middle cerebral artery. INTERVENTIONS: The patient was administered hyperbaric oxygen, antiplatelet aggregation therapy, and dehydration treatment. OUTCOMES: Clinical death occurred 55 hours after air embolism. LESSONS: Systemic air embolism is a serious complication of lung puncture. Clinicians should improve their understanding of this complication and remain vigilant against air embolism.

Review: cerebral amyloid angiopathy, prion angiopathy, CADASIL and the spectrum of protein elimination failure angiopathies (PEFA) in neurodegenerative disease with a focus on therapy.

Failure of elimination of proteins from the brain is a major feature in many neurodegenerative diseases. Insoluble proteins accumulate in brain parenchyma and in walls of cerebral capillaries and arteries. Cerebral amyloid angiopathy (CAA) is a descriptive term for amyloid in vessel walls. Here, we adopt the term protein elimination failure angiopathy (PEFA) to focus on mechanisms involved in the pathogenesis of a spectrum of disorders that exhibit both unique and common features of protein accumulation in blood vessel walls. We review (a) normal pathways and mechanisms by which proteins and other soluble metabolites are eliminated from the brain along 100- to 150-nm-thick basement membranes in walls of cerebral capillaries and arteries that serve as routes for lymphatic drainage of the brain; (b) a spectrum of proteins involved in PEFA; and (c) changes that occur in artery walls and contribute to failure of protein elimination. We use accumulation of amyloid beta (Aß), prion protein and granular osmiophilic material (GOM) in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) as examples of different factors involved in the aetiology and pathogenesis of PEFA. Finally, we discuss how knowledge of factors involved in PEFA may help to focus on new therapies for neurodegenerative diseases. When Aß (following immunotherapy) and prion protein are released from brain parenchyma they deposit in walls of cerebral capillaries and arteries; GOM in CADASIL accumulates primarily in artery walls. Therefore, the focus of therapy for protein clearance in neurodegenerative disease should perhaps be on facilitating perivascular elimination of proteins and reducing PEFA.

Traumatic arteriovenous fistula of the superficial temporal artery: a histopathologic report.

Traumatic aneurysms, pseudoaneurysms, and arteriovenous (AV) fistulas of the superficial temporal artery (STA) are uncommon, accounting for only 0.5% to 2.0% of all aneurysms subjected to surgery. In the literature that relates to the STA, the general term "aneurysm following traumatic injury" often includes a wide array of pathologic entities, including proper aneurysms, pseudoaneurysms, and AV fistulas. In 75% of cases, such aneurysms are due to blunt trauma. Within this group, STA AV fistulas constitute an exceedingly rare subset. The case presents the occurrence of a traumatic AV fistula of the STA following blunt trauma (karate kick) and provides the first description of the histologic appearance of this lesion.

Factors associated with favorable response to hyperbaric oxygen therapy among patients presenting with iatrogenic cerebral arterial gas embolism.

BACKGROUND: Iatrogenic cerebral arterial gas embolism (CAGE) is an uncommon but potentially a fatal condition. Hyperbaric oxygen (HBO2) therapy is the only definitive treatment for patients with CAGE presenting with acute neurologic deficits. METHODS: We reviewed medical records and neuroimaging of consecutive CAGE patients treated with HBO2 at a state referral hyperbaric facility over a 22-year period. We analyzed the effect of demographics, source of intra-arterial gas, signs and symptoms, results of imaging studies, time between event and HBO2 treatment, and response to HBO2 treatment in 36 consecutive patients. Favorable outcome was defined by complete resolution or improvement of CAGE signs and symptoms at 24 h after HBO2 treatment. Unfavorable outcome was defined by unchanged or worsened neurologic signs and symptoms or in hospital death. RESULTS: A total of 26 (72%) of the 36 patients had favorable outcome. Patients with favorable outcome were younger compared to those with unfavorable outcome (mean age [years, SD] 44.7 ± 17.8 vs. 58.1 ± 24.1, p = 0.08). Cardiopulmonary symptoms were significantly more common in CAGE related to venous source of gas compared to arterial source (p = 0.024) but did not influence the rate of favorable outcomes. Adjusted multivariate analysis demonstrated that time from event to HBO2 ≤ 6 h (positively) and the presence of infarct/edema on head computerized tomography (CT)/magnetic resonance imaging (MRI) before HBO2 (negatively) were independent predictors of favorable outcome at 24 h after HBO2 treatment [odds ratio (OR) 9.08 confidence interval (CI) (1.13-72.69), p = 0.0376, and (OR) 0.034 (CI) (0.002-0.58), p = 0.0200, respectively]. Two of the 36 patients were treated with thrombolytics because of acute focal deficits and suspected ischemia-one with intravenous and the second with intra-arterial thrombolysis. The latter patient developed fatal intracerebral hemorrhage. CONCLUSIONS: A high proportion of CAGE patients treated with HBO2 had favorable outcomes. Time-to-HBO2 ≤ 6 h increased the odds of favorable outcome, whereas the presence of infarct/edema on CT/MRI scan before HBO2 reduced the odds of a favorable outcome. Timely diagnosis and differentiation from thrombo-embolic ischemic events appears to be an important determinant of successful HBO2 treatment.

Pulmonary barotrauma and cerebral arterial gas embolism during hyperbaric oxygen therapy.

Hyperbaric oxygen therapy (HBOT) is used to treat a variety of disorders. It is a safe treatment modality, but rare catastrophic complications may occur. In this case report, we describe the occurrence of irreversible spastic quadriparesis in a patient who suffered a cerebral arterial gas embolism (CAGE) during decompression from HBOT. The patient had a history of respiratory disease and was subsequently found to have bullous changes in the left lung, which almost certainly predisposed to this rare event. We discuss appropriate pretreatment screening to prevent such events and highlight the paradox that HBOT, the cause of the CAGE, is also the treatment of choice.

Pulmonary barotrauma-induced cerebral arterial gas embolism with spontaneous recovery: commentary on the rationale for therapeutic compression.

Pulmonary barotrauma-induced cerebral arterial gas embolism (CAGE) continues to complicate compressed gas diving activities. Inadequate lung ventilation secondary to inadvertent breath holding or rapid buoyant ascent can quickly generate a critical state of lung over-pressure. Pulmonary over-pressurization may also occur as a consequence of acute and chronic pulmonary pathologies. Resulting barotrauma frequently causes structural failure within the terminal distal airway. Respiratory gases are then free to embolize the systemic circulation via the pulmonary vasculature and the left heart. The brain is a common target organ. Bubbles that enter the cerebral arteries coalesce to form columns of gas as the vascular network narrows. Small amounts of gas frequently pass directly through the cerebral circulation without occlusion. Larger columns of gas occlude regional brain blood flow, either transiently or permanently, producing a stroke-like clinical picture. In cases of spontaneous redistribution, a period of apparent recovery is frequently followed by relapse. The etiology of relapse appears to be multifactoral, and chiefly the consequence of a failure of reperfusion. Prediction of who will relapse is not possible, and any such relapse is of ominous prognostic significance. It is advisable, therefore, that CAGE patients who undergo spontaneous recovery be promptly recompressed while breathing oxygen. Therapeutic compression will serve to antagonize leukocyte-mediated ischemia-reperfusion injury; limit potential re-embolization of brain blood flow, secondary to further leakage from the original pulmonary lesion or recirculation of gas from the initial occlusive event; protect against embolic injury to other organs; aid in the resolution of component cerebral edema; reduce the likelihood of late brain infarction reported in patients who have undergone spontaneous clinical recovery; and prophylax against decompression sickness in high gas loading dives that precede accelerated ascents and omitted stage decompression.

Vertebral artery injury presenting with signs of middle cerebral artery occlusion. A case report.

Therapeutic manipulation of the neck has been shown to produced injury to the vertebral artery. The clinical syndromes produced by this arterial insufficiency generally reflect dysfunction of the brainstem or cerebellum. The authors present a case of such injury that presented with clinical findings, namely, hemiparesis and aphasia, suggestive of involvement of the dominant middle cerebral artery. These findings may have been the result of disruption of flow through the posterior cerebral artery to the thalamus, internal capsule, and cerebral peduncles.

Intracranial arterial occlusion associated with high-activity iodine-125 brachytherapy for glioblastoma.

We describe two patients who developed devastating strokes due to intracranial arterial occlusion 15 weeks and 97 weeks following high dose stereotactic iodine-125 brachytherapy for glioblastoma multiforme. In both cases the occlusion was within the implant volume at points receiving 110-281 Gy and there was no other evidence of significant atherosclerosis in the patients. We therefore conclude that these complications were a direct result of the brachytherapy. The phenomenon of radiation-induced occlusion of large cerebral arteries is reviewed.

[Experience with nimodipine treatment of vascular spasm after subarachnoid hemorrhage]. / Wlasne doswiadczenia w leczeniu nimodypina skurczu naczyniowego po krwotokach podpajeczynówkowych.

Pathogenesis of vasospasms following subarachnoid haemorrhage and possible therapeutic efficacy of nimodipine (calcium channel blocking agent) are discussed. The authors present their own experience in the treatment of 209 patients with subarachnoid haemorrhage with nimodipine. Collected clinical results suggest the necessity of the combined treatment of vasospasm following subarachnoid haemorrhage with nimodipine, hypervolemia, and hypertensive agents.

[Occlusion of a perforating artery, by descending tentorial herniation after head injury, supplying deep cerebral structure--report of 4 cases and their CT evaluation].

Four cases with descending tentorial herniation (DTH) after head injury which showed thalamic, mesencephalic and basal ganglionic low density areas (LDAs) manifesting a infarction in postoperative CT films are reported, and a possible mechanism are discussed in this paper. Case 1: Bilateral acute subdural hematoma with left DTH showed LDAs in the anterior part of the bilateral thalami, left occipital lobe and midbrain. The estimated occluded arteries included the anterior thalamoperforating artery(AThA), posterior cerebral artery and midbrain perforator. Case 2: Right acute epidural hematoma with DTH showed LDAs in the anterior part of the right thalamus and in the left globus pallidus. The estimated occluded arteries included the AThA and anterior choroidal artery. Case 3: Right acute epidural hematoma with DTH showed LDAs in the anterior part of the left thalamus, and in the left midbrain tegmentum. The estimated occluded artery was the interpeduncular thalamoperforating artery (IThA). Case 4: Right chronic subdural hematoma with DTH showed LDA mainly in the left thalamus except for the superior thalamic region. The estimated occluded arteries included the AThA and/or IThA and thalamogeniculate artery. Cases 1 and 4 were adult males and cases 2 and 3 were infant males, and the prognosis was good in the infant males, and poor in the adult males. Each of the 4 cases showed no loss of consciousness just after the head injury while 3 out of them deteriorated within several hours, and one was a case of chronic subdural hematoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral arterial air embolism: I. Is there benefit in beginning HBO treatment at 6 bar?

A method for studying treatment of cerebral arterial gas embolism in dogs is described. The model produces severe cortical dysfunction and cerebral blood flow deficits. The efficacy of treatment was assessed using median nerve somatosensory cortical evoked potentials (CEP), [14C]iodoantipyrene autoradiographic cerebral blood flow studies, brain water content, and various physiological parameters. A direct comparison of modified U.S. Navy Treatment Tables 6 and 6A is reported. Complete recovery of CEP was not seen after 90 min of treatment. The maximum rate of CEP recovery occurred in the first 15 min of treatment. Recovery continued out to 60 min. Thereafter, some dogs on treatment 6A showed signs of deterioration. The cerebral blood flow studies were the same in both groups and showed no sign of pathologically low levels of flow. It appeared that there was no advantage in preceding 2.8-bar (60-ft) oxygen treatments with compression to 6 bar (165 ft) on air for the treatment of arterial air embolism in this model.

Experimental treatment of cerebral vascular spasm secondary to subarachnoid hemorrhage.

Cerebral artery spasm following subarachnoid hemorrhage (SAH) is a major cause of morbidity and mortality. Treatment or prevention methods are most desirable. Using the basilar artery of the rabbit, cerebral arterial spasm was induced with an injection of 4 ml of autologous blood via cisternal puncture in six treated, four pre-treated and six control animals. Vertebral angiography was performed before and at ten, twenty, thirty and sixty minutes after the injection of blood was carried out, and the presence of spasm and its cause were followed in these animals. Pre-treated and treated subjects received 2 mg/kg of diltiazem (a calcium antagonist) either before and after the injection of blood, respectively. Analysis of vessel diameters by computer assisted densitometry showed that the treated group had a significant reduction of basilar artery spasm when compared to the control group, while in the pre-treated group, spasm was prevented.

Cerebral arterial spasm: part 10. Reversal of acute and chronic spasm in dogs with orally administered nifedipine.

In vivo experiments in dogs demonstrated angiographically that the subarachnoid injection of blood produced cerebral arterial apasm both immediately after the injection of blood and 2 days later. The sublingual adminstration of nifedipine reversed both the acute and the delayed cerebral arterial spasm. In addition, sublingual administration of nifedipine 20 minutes before the subarachnoid injection of blood prevented the acute spasm.

Prostaglandins. A review of neurophysiology and psychiatric implications.

This article reviews the function of prostaglandins (PGs) in the nervous system and discusses the possible alterations in PG metabolism as relating to mental illness. The PGs are a unique group of cyclic fatty acids whose immediate precursors are thought to function postsynaptically by inhibition or facillitation of neurotransmission through cyclase inhibition or activation, and by means of a negative feedback loop to inhibit further release of neurotransmitter from the presynaptic nerve. A review of PGs in psychiatric conditions is presented as well as a discussion of the interaction of psychoactive drugs with the PGs. The concluding section of this review discusses possible future strategies to provide insight into PG physiology as it relates to synaptic transmission in normal and pathological conditions in man.

Radio-frequency thrombosis of vascular malformations with a transvascular magnetic catheter.

A tiny magnetic electrode catheter introduced into the human carotid artery has been mechanically and magnetically propelled, with fluoroscopic control, to cranial arteriovenous malformations. Radio-frequency heating of the catheter tip in successive positions occludes abnormal blood vessels.