Basal ganglia hemorrhagic lesions following trauma are relatively rare and are reported in 0.9%–3.0% of head traumas [1, 2]. Striatocapsular infarction (SCI) after trauma is a rare event [3, 4, 5]. Differentiation of traumatic or non-traumatic SCI can be important in forensic medicine. Most cases of ischemic infarction in the basal ganglia (BG) after trauma have been reported in young children [6, 7, 8]. We found only five cases of post-traumatic SCI in adult patients [9, 10, 11, 12, 13]. In adult patients without any stroke risk factors, trauma must be included in probable etiology [9]. Although some have suggested damage to the lenticulostriate artery (LSA) after trauma [11, 12, 13], the mechanism of infarction in the BG following trauma remains unclear. We reviewed articles for post-traumatic SCI caused by damage to multiple LSAs and those with spontaneous SCI. We excluded SCI due to traumatic arterial dissection and thrombus in the middle cerebral artery (MCA).

Head trauma is rarely cited as an etiology of infarction in the BG. In adults and pediatric patients, arterial dissection can result in ischemic events after trauma [14, 15, 16, 17]. Trauma from football and other sports results in arterial dissection with thromboembolism of the brain [14]. Dissection of vessels with cerebral embolism to distal territory can be developed after a traumatic event [18].

However, cases of post-traumatic SCI without vessel dissection have been reported in some adults (Table 1, Ref. [9, 10, 11, 12, 13]). The combination of subarachnoid hemorrhage (SAH), hemorrhage, and infarction of the BG due to ruptured LSA after trauma has been reported in only two cases [11, 13]. In these two patients, other causes for SAH and ischemia, such as aneurysm or arterial-dissection, were not detected with magnetic resonance (MR) imaging or cerebral angiography. In these two patients, the size of the ischemic lesion in the BG was larger than 1.5 cm [11, 13].

The BG and internal capsule are perfused by the LSA. These vessels are end arteries. Therefore, the area they perfuse are at risk for ischemia [19]. Any violent motion of the head may result in damage of the vessel between the subarachnoid part of LSA and the intraparenchymal section of the LSA [20]. Inertia from trauma on the skull can also result in movement of brain tissue and damage to intracranial vessels [6]. This movement leads to a traumatic intimal lesion following the generation of a thrombus. This thrombus causes ischemia in the cerebral tissue. Maki et al. [20] suggested that when a stretching force is severe, vessel walls can rupture and lead to cerebral hemorrhage, whereas milder damage may only cause endothelial injury and ischemic stroke. Although the case presented was in a young patient, Ahn et al. [21] reported that a punctate high-density lesion detected with a computed tomography (CT) scan 2 h following injury indicates a thrombus in the LSA. In the case presentation by Ahn et al. [21], repeat CT after the development of hemiparesis demonstrated a discrete infarction around a focal, high-density region. To our knowledge, this description is the first report suggesting a thrombus after trauma. Direct visualization of LSA damage after trauma was reported by Kim et al. [12]. An angiographic evaluation of intracranial vessels in four of five cases in adults with post-traumatic BG infarction did not demonstrate damage to the LSA despite CT angiography [9, 10], MR angiography [13], or cerebral angiography [11]. Only one of five cases in adults with post-traumatic SCI demonstrated structural damage in the LSA by cerebral angiography and MR angiography [12]. Perhaps the incidence of this mechanism in head trauma is rare and detailed documentation may identify more traumatic causes for stroke [6].

Most cases of post-traumatic SCI due to LSA damage have been reported in children. In the event of a BG infarction in a young child following head trauma, the etiology is often the result of anatomical characteristics at this age [22]. For example, the LSAs form sharp angles with the MCA, which is more acute in children than adults [20, 23]. Anatomically, between the intracerebral and the subarachnoid segment of the LSAs, there is a mobile subarachnoid segment, that when stretched and distorted by trauma, results in ischemic lesion in the area of LSAs. Additionally, the sphenoid bone in children is developing and not fully ossified. The brain parenchyma has greater mobility than the skull during violent trauma. Moreover, the subarachnoid space in children is smaller and less protected from trauma than in adults. These factors facilitate the stretching of LSAs by traumatic forces [4, 24]. Cerebral blood flow in the first five years increases to twice that of an adult. Thus, children are more susceptible and sensitive to cerebral hypoxia. In young children, even mild head trauma could result in BG infarction [22, 25, 26, 27].

The damage of a deep perforator vessel in the brain can cause a lacunar infarction with a diameter of 1.5 cm [28]. Perforating infarcts with a diameter larger than 1.5 cm in the LSA territory can develop from the occlusion of a main stem perforator or simultaneous damage from multiple perforators [29]. Among ischemic lesions in the BG, large subcortical lesions with a size $>$3 cm are classified as a SCI [30]. The clinical presentations of a SCI typically include hemiparesis, language problems, sensory neglect, or apraxia [31].

Following a study conducted by Bladin and Berkovic [32], SCIs were classified as a subtype of ischemia. The ischemic lesions of SCI were located in territories of the LSAs and could extend to territories of the Heubner or anterior choroidal arteries [33, 34, 35]. Jose and James [36] proposed classifying ischemic stroke into 10 subtypes. Of the 10 infarction subtypes, SCI is considered a subcortical infarction in the striatocapsular portion, developed following damage to more than one LSA [36]. According to its radiological findings, especially on axial images, these SCIs are lentiform, triangular, or comma-shaped. The size of a SCI is 3–4.5 cm, 1–2 cm wide and 2–4 cm in depth. The impacted infarction regions include the caudate nucleus, putamen, and anterior limb of the internal capsule. The globus pallidus, genu, and posterior limb of the internal capsule are not typically affected. The comma-shaped lesions involve the caudate nucleus along with the anterior limb of the internal capsule and the lentiform nucleus [36]. Cardiac problems, severe carotid artery stenosis, and atherosclerotic disease affecting the proximal MCA are other important causes of SCI [3, 32, 33, 37, 38, 39, 40].

Lee et al. [41] reported that the dominant portion of SCI on coronal diffusion MR was important for identification of stroke cause. Stroke resulting from a proximal embolism, such as those with cardiac origin, is more prevalent in patients with a lesion distributed equally between the distal and proximal perfusion areas of the LSA. By contrast, MCA stenoses resulting in SCI are more common in patients with a lesion distributed predominantly in the distal perfusion area of LSA [42].

Of five adult patients with post-traumatic SCI, we could evaluate the dominant infarction area of the SCI in only three. In these three patients with traumatic SCI due to LSA damage [11, 12, 13], the dominant infarcation area was located in the distal perfusion area of the LSA, similar to the SCI associated with symptomatic MCA stenoses.

Although direct visualization of damage to the LSAs by trauma is difficult, assessing the injury is important when evaluating SCI after trauma. It is difficult to image the entire proximal-to-distal LSA using angiography. At present, there is no imaging technique that can display the LSAs clearly and directly in clinical settings. Ultrahigh-resolution CT is a useful method for evaluating the LSAs [43]. LSA imaging has clinical implications for differentiating between spontaneous and traumatic origins in patients with BG infarction.

Vessel Wall Imaging (VWI) may provide useful information for differentiating the etiology of SCI. VWI can provide a reliable tool for identifying intracranial vessel plaques in vivo [44, 45]. Enhancement after gadolinium within an intracranial vessel plaque can suggest a strong association with ischemia [46]. VWI could be used to provide evidence of dissection flap with thrombi [47]. Intramural hematoma is a frequent imaging finding following cervicocerebral artery dissection and can also be imaged using VWI [48].

Post-traumatic SCI due to LSA damage in adults could be associated with a hemorrhage in the BG. Therefore, we reviewed the simultaneous occurrence of spontaneous infarction and hemorrhage in adults. Stroke is classified as either an ischemic and hemorrhagic stroke. Usually, a stroke will present as only one type, whereas the simultaneous development of ischemia and hemorrhage is rare. Hypertensive brain hemorrhage and lacunar infarction are developed from common damage to small perforating arteries. Hypertension is a condition commonly underlying primary intracerebral hemorrhage and lacunar infarction. However, the infarction and hemorrhage rarely occur simultaneously [49]. There are a few documented cases of infarction and hemorrhage developed simultaneously in the literature [49, 50, 51, 52]. These patients with simultaneous infarction and hemorrhage had no trauma history but had underlying risk factors for cerebral stroke.

We observed simultaneous development of BG infarction and hemorrhage in four of five adult cases of post-traumatic BG infarction [10, 11, 12, 13]. In adult patients, the simultaneous development of BG infarction and hemorrhage in the LSAs is important for the differentiation of traumatic or non-traumatic origins.

In case of SCI infarction associated with hemorrhage in LSA territory after trauma, we should distinguish sequential spontaneous occurrence of BG hemorrhage and ischemia in the LSA perfusion area. To our knowledge, only one case of the sequential occurrence of BG hemorrhage and infarction in the LSA territory has been reported [53]. An 82-year-old woman with hypertension and no history of trauma presented with right hemiparesis due to putaminal hemorrhage. The left internal capsule and corona radiata were normal on a an initial CT scan and blood pressure medication was started. On day two, the right hemiparesis progressed to right hemiplegia. CT demonstrated no change of the hematoma volume, but the left corona radiata showed a low-density area. On day six, MR imaging showed corona radiata ischemia. Intensive blood pressure-lowering therapy may result in ischemic damage. Careful observation of neurological status and repeat imaging can suggest differentiation between spontaneous BG hemorrhage followed by infarction in the same LSA territory and trauma associated with the simultaneous development of BG infarction and hemorrhage.

Post-traumatic SCI due to LSA damage in adults might be associated with hemorrhage in the BG. Careful observation of neurological status and the use of imaging can be used to differentiate between simultaneous and sequential development of BG infarction and hemorrhage. In cases with no risk factors for stroke, simultaneous post-traumatic development of infarction and hemorrhage in the same LSA territory might suggest a traumatic origin.

BG, basal ganglia; CT, computed tomography; LSA, lenticulostriate artery; MCA, middle cerebral artery; MR, magnetic resonance; SAH, subarachnoid hemorrhage; SCI, striatocapsular infarction; VWI, vessel wall imaging.

JUM and MSK designed the research study, collect and sort references, wrote and revised the manuscript. YHK and MK reported similar cases and critically revised the manuscript. MSK designed this review article. All authors contributed to editorial changes in the manuscript. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

Not applicable.

Thanks to all the peer reviewers for their opinions and suggestions.

This research received fees for English correction and publication from National Medical Center located in Seoul, Republic of Korea.

The authors declare no conflict of interest.