Posttraumatic Vasospasm: Is It Important?

Zubkov A. Y.

University of Mississippi Medical Center, Jackson, MS, USA

Cerebral vasospasm is one of the leading causes of mortality and morbidity after subarachnoid hemorrhage (SAH). Cerebral vasospasm can develop in patients with head injury, as well. This paper will present the review of current knowledge in posttraumatic vasospasm (PTV).

Cerebral PTV was first described by Lorn in 1936 [16]. In 1963, two articles appeared almost simultaneously, one by Freidenfelt and Sundstrom [9] describing five cases and another by Columnella [6], who found that PTV could be observed in 10% of angiograms performed in patients with head injury. In that study author distinguished between general and localized arterial spasm.

In 1972 Suwanwela et al. studied 350 patients with head injury and found narrowing of one or more intracranial vessels in 18.6% of cases [27]. They recognized four types of arterial narrowing in association with acute head injury: (a) localized narrowing of major cerebral arteries at the base of the brain in 5.1%; (b) localized narrowing of branches of the cerebral arteries at the site of the cerebral contusion in 9.5%; (c) diffuse narrowing of the cerebral arteries in 3.4%; and (d) spasm, associated with penetrating injury of the cerebral arteries.

During this early period, investigators found that PTV could be discerned on angiograms in 5-33% of the cases [4,6,16,27,33]. However, it was obvious that angiography could not sufficiently describe the actual incidence of PTV. In head injury cases angiography was performed mainly in the first days after injury and subsequently only in cases of deterioration of the patient’s condition. With the development of computerized tomography (CT), angiography has been used less frequently in head injury patients.

In 1982, Aaslid introduced a new method of investigation of intracranial arteries, transcranial Doppler ultrasonography (TCD) [1]. With this effective diagnostic tool available to clinicians, the incidence of recognized and reported PTV has risen to 26.7-68% [7,10,14,21,24,25,31,34].

ETIOLOGY AND PATHOGENESIS

From studies of vasospasm after aneurysmal rupture it is well known that the amount of subarachnoid blood correlates strongly with severity of vasoconstriction. In a cooperative study of the National Institutes of Health, based on CT examinations of 753 patients with severe head injury, subarachnoid hemorrhage appears in 40% of patients [12].

Study from the University of Mississippi Medical Center demonstrated that in 68.7% of the patients with PTV, head injury was complicated by traumatic SAH (tSAH). At the same time tSAH was not detected on CT in 31.3% of patients with PTV [37]. Other studies revealed that PTV was accompanied by tSAH in 90% of cases. Martin et al. showed that three CT findings, tSAH, subdural hematoma, and intracerebral hemorrhage, were independent predictors of middle cerebral artery (MCA) spasm [21]. The likelihood of developing vasospasm was 14% in the presence of one of these factors, but if two of these factors were present the possibility became 65-78%. Similar results were obtained by Zubkov et al.[37]. He demonstrated that epidural and subdural hematomas were more frequent in the patients with PTV. It is possible that these facts only evidenced more severe head injury in patients with PTV.

Many authors underlined similarities in PTV and vasospasm occurring after aneurysm rupture, assuming similar pathogenesis. This certainly is true for PTV accompanied by subarachnoid hemorrhage, but in 10-30% of cases PTV occurs without any visible blood in the CSF. The significance of mechanical factors for development of PTV received attention from several investigators.

Arseni concluded that contusion of the carotid artery in the cavernous sinus is an important pathogenetic factor for PTV [2]. Echlin showed that cerebral vasospasm may occur after head injury even with clear cerebrospinal fluid [8]. The possibility that an injurious stimulus (trauma) to an artery may act as a chronic or long-lasting stimulus should be considered. Lewin [17] emphasized that the origin of the middle cerebral artery and particularly its temporal branches are especially vulnerable as they leave the basal subarachnoid space, where they could be injured against the sphenoid bone. On the other hand Arutiunov [3] found that mechanical stimuli were capable of producing only short-term vasospasm.

Inflammation is considered one of the important pathogenetic factors responsible for the development of vasospasm. Cerebral vasospasm can develop in patients with meningitis [26,35]. Significance of inflammation was suggested by demonstration of increased inteleukins concentration in the cerebrospinal fluid of the patients with SAH [32], by increased collagen deposition in the vessel wall [22], and by limited effects of anti-inflammatory drugs on the cause of experimental vasospasm [36]. Inflammatory complications of head injury are well documented and might be involved in the pathogenesis of PTV.

CLINICAL SIGNIFICANCE

Posttraumatic vasospasm certainly plays a role in patient outcome. Macpherson and Graham found vasospasm in 41% of patients who died from head injury. They found ischemia of cerebral hemispheres in 51% of cases as compared to 32% with vasospasm without ischemia [18,19].

Taneda et al. found that ischemic symptoms directly attributable to vasospasm occurred in 7.7% of patients [28]. In a group of patients with massive tSAH, 24.1% developed ischemic symptoms, in contrast to 3.0% of patients with mild tSAH. Vasospasm was found in 20% of patients with mild tSAH and 63% of patients with massive tSAH. They found ischemic symptoms accompanying cerebral arterial spasm following tSAH comparable to those found following aneurysmal SAH.

Using TCD, vasospasm may be found in head injury patients from 12 hours to 4 days after head injury and with duration from 12 hours to 14 days [7,37]. Sanders showed that vasospasm might appear between the third and fifth days [25], although PTV can be demonstrated by TCD even on the second day after injury [37]. Our study demonstrated that 20.8% of the patients developed vasospasm within 3 days after head injury. At the same time, the duration of vasospasm was more than 3 days in 58.3% [39]. According to Weber et al., increases in velocities began during the first 48 hours and reached maximum values between the fifth and seventh days [31].

Only a few authors have studied posterior circulation vasospasm in head injury patients. Marshall described 6 cases and showed that this spasm may be primarily responsible for brainstem dysfunction [20]. Using TCD measurements Martin found that 1/3 of head injury patients had vasospasm in both arterial circulations [21]. None of the patients with both locations of PTV had favorable outcome. Hadani et al. found 70% incidence of basilar artery PTV in severe head injury and 40% incidence in moderate head injury [11]. 90% of patients with BA PTV died.

MORPHOLOGIC CHANGES

Only two studies have so far reported morphologic changes in cerebral arteries in patients with PTV. Hughes described morphological changes in 10 cases of head injury [13]. He defined the presence of vasospasm if the tunica media of arterial wall was fibrotic and thinner than normal and if there was a concentric layer of subendothelial fibrous tissue completely encircling the lumen. The author divided these changes into 4 groups, including: (a) tunica media atrophy with gross subendothelial thickening (over 0.2 mm); (b) subendothelial thickening of 0.1-0.2 mm; (c) subendothelial thickening of 0.1 mm; (d) tunica media atrophy indistinct or subendothelial fibrosis not fully encircling the lumen. These changes in posterior circulation arteries were taken as evidence for vertebrobasilar vasospasm as cause of death in head injury patients.

Zubkov et al. studied development of PTV with TCD. Morphologic changes in the vessels of head injury patients were similar to vasospasm pattern seen in the post-aneurysmal SAH vasospasm. Apoptosis and desquamation of endothelial cells, thickening of the subintimal layer, fibrosis of muscle layer were typical for both types of vasospasm [38,39].

TREATMENT

There have been several studies during which attempts were made to treat PTV. Koston found that nimodipine had a positive effect on PTV and improved physiological brain functions after head injury [15]. However, Bailey [5] and the European Nimodipine Study in 1994 [29] found opposite results, with nimodipine of minor clinical effectiveness after head injury. Newell performed angioplasty in one patient with severe PTV with good results [23]. Vardiman described the successful use of smooth muscle relaxant papaverine in the treatment of severe PTV [30].

CONCLUSIONS

Posttraumatic vasospasm is a well defined pathology that develops after head injury, and significantly complicates it’s course. Clinical presentation of PTV is different from post-aneurysmal SAH vasospasm. PTV tends to develop early and to have a short course. Morphological presentation of both types of vasospasm is similar. Despite these similarities the pathogenesis of PTV might be different and requires further investigation.

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