Keywords
basal ganglia - craniocerebral trauma - neuroimaging - traumatic cerebral hemorrhage
Palavras-chave
gânglios da base - hemorragia traumática cerebral - neuroimagem - trauma craniocerebral
Introduction
Basal ganglia traumatic hematoma (BGTH) is characterized by being in the basal ganglia
(caudate nucleus, putamen and globus pallidus) or in adjacent structures, such as
the thalamus and the internal capsule.[1]
[2] The basal ganglia hematoma often occurs spontaneously in hypertensive patients,
and it is rarely caused by trauma; it is associated with a poor prognosis[3] and severe injuries.[4] Basal ganglia traumatic hematomas represent 3.2% in closed traumatic brain injuries
(TBIs).[5] It often occurs in high-speed trauma, and falls from heights are one of the causes
of pediatric BGTH.[6] Basal ganglia (BG) hematomas > 2 cm are considered large,[7]
[8] and those with diameter < 2 cm can be considered a hemorrhage due to cerebral contusion,[9] associated as part of the spectrum present in diffuse axonal injury (DAI).[5] Basal ganglia deep cerebral contusion and brain gray matter deep region are classified
as intermediary contusion, characteristic of DAI.[10] Basal ganglia traumatic hematoma patients have a high incidence of coagulating disorders,
DAI, contusion, intraventricular hemorrhage, and extra axial hematomas.[1]
The authors present a series of 16 BGTH cases, describing its causes, treatment, and
results.
Patients and Methods
This is a retrospective study of 16 patients diagnosed with basal BGTH, aged 16 to
44 years, admitted to Hospital de Urgência de Sergipe (Aracaju, SE, Brazil), in the
period from 2009 to 2013. The following aspects were analyzed: age, gender, injury
laterality, injured basal ganglia, imaging tests, treatment, and prognosis.
The literature review was performed according to the preferred reporting items for
systematic reviews and meta-analyses (PRISMA) statement. The inclusion criteria were
studies and case reports with a time frame between 1986 and 2019, with individuals
of any determined age group, diagnosed with BGTH. Studies not developed in humans,
published in databases with no abstract, systematic reviews, and letters to the editor,
were excluded.
The literature review was performed in July 12, 2020 using the following databases:
PubMed, ScienceDirect, and Google Scholar, using the terms craniocerebral trauma AND basal ganglia and basal ganglia AND hematoma AND trauma. Duplicate studies were removed, resulting in a total of 19 articles that met the
inclusion criteria taking into account their citations and their respective impacts.
Results
In the present case series, all patients were male, with a mean age of 21 years and
5 months. The main causes of BGTH were traffic accident (12) and accidental fall (3)
([Table 1]). The mean Glasgow coma scale (GCS) score on admission was 8. All patients underwent
a computed tomography (CT) test, showing that the main affected nuclei were the putamen
(5), the caudate nucleus (4), and the internal capsule (4) ([Figures 1],[2],[3],[4],[5],[6],[7],[8],[9]). In the analysis of the laterality of the lesion, in five patients the lesion was
located on the right side, in five it was on the left side, and in six, there were
lesions on both sides ([Table 2]). Thirteen patients underwent conservative treatment and three underwent intracranial
hematomas drainage—two epidural hematomas (EDH), and one subdural hematoma (SDH).
Seven patients survived, four had neurological sequelae, and nine patients died.
Table 1
Clinical-epidemiological characteristics of 16 BGTH patients
Clinical-epidemiological characteristics (n = 16)
|
Characteristics
|
No.
|
Percentage
|
Sex
|
|
|
Male
|
16
|
100%
|
Female
|
0
|
0.00%
|
Causes
|
|
|
Traffic accident
|
12
|
75.00%
|
Accident fall
|
3
|
18.75%
|
Physical aggression
|
1
|
6.25%
|
Treatment
|
|
|
Surgical
|
3
|
18.75%
|
Conservative
|
13
|
81.25%
|
Results
|
|
|
Good general condition
|
3
|
18.75%
|
Neurological sequelae
|
4
|
25.00%
|
Death
|
9
|
56.25%
|
Fig. 1 Skull computed tomography without contrast showing acute epidural hematoma in the
left temporoparietal region and frontal contusion hematoma in left basal ganglia.
Fig. 2 Non-contrast skull computed tomography showing bilateral basal ganglia hematoma.
Fig. 3 Non-contrast skull computed tomography showing hemorrhage in the right lateral ventricle
associated with left basal ganglia hematoma.
Fig. 4 Non-contrast skull computed tomography showing right parietal hematoma, left temporal
contusion and left basal ganglia hematoma.
Fig. 5 Non-contrast skull computed tomography showing bilateral lesion in basal ganglia.
Fig. 6 Computed tomography of the skull without contrast with large right basal ganglia
hematoma and compression of the right lateral ventricle, with deviation of the midline
structures.
Fig. 7 Computed tomography of the skull without contrast with hematoma in left basal ganglia.
Fig. 8 Non-contrast skull computed tomography showing left acute frontoparietal subdural
hematoma, intraventricular hemorrhage, deviation of the midline structures and right
basal ganglia hematoma.
Fig. 9 Non-contrast skull computed tomography showing intraventricular hemorrhage, subarachnoid
hemorrhage, massive left basal ganglia hematoma.
Table 2
Skull computed tomography of 16 BGTH patients
Characteristics of skull computed tomography (n = 16)
|
Characteristics
|
No.
|
Percetage
|
Lateralization
|
|
|
Right
|
5
|
31.25%
|
Left
|
5
|
31.25%
|
Bilateral
|
6
|
37.5%
|
Associated injuries
|
|
|
Subdural hematoma
|
3
|
18.75%
|
Epidural hematoma
|
2
|
12.25%
|
Cerebral contusion
|
5
|
31.25%
|
Diffuse axonal injury
|
4
|
25.00%
|
Basal ganglia hematoma location
|
|
|
Putamen
|
5
|
31.25%
|
Caudado nucleus
|
4
|
25.00%
|
Internal capsule
|
4
|
25.00%
|
Globus pallidus
|
2
|
12.25%
|
Thalamus
|
1
|
6.25%
|
Discussion
Epidemiology
Basal ganglia TBIs in closed cranial lesions represent 3%,[1]
[6]
[8] and, when found in autopsies, they represent 10%.[3] In a study Moe et al., it was demonstrated that when associated with DAI affecting
unilateral and bilateral BG, they represent 18% and 2%, respectively,[11] being extremely rare in the pediatric population.[9] Chung et al.,[4] in a study with 309 pediatric TBI patients, showed that all BG lesions were unilateral
and represented only 2.5%.
Basal ganglia traumatic hematoma is often small, uni or bilateral, located in the
internal capsule and lenticular nucleus (putamen and globus pallidus),[2] which may occur in the thalamus and caudate nucleus,[12] and it may be accompanied by cranial fracture, brain stem lesions, subarachnoid
hematoma,[3] EDH, and SDH.[8] When the hematoma occurs due to spontaneous hemorrhage, it is unilateral and commonly
located in the internal capsule and thalamus.[2] Jayakumar et al.,[13] in a study with 22 patients, showed the following location distribution of BGTH:
41% in the putamen, 23% in the caudate nucleus, 23% in the internal capsule, and 13%
in the thalamus, with the highest mortality associated with the first structure.
In the present study, 10 lesions were located unilaterally and 6 bilaterally. The
affected nuclei were the putamen (5), caudate nucleus (4), internal capsule (4), globus
pallidus (2), and thalamus (1). The associated injuries were SDH (3), EDH (2), brain
contusion (5), and DAI (4).
Physiopathology
It is believed that BGTH occurs due to shear forces.[5] When there is a high-energy impact on the vertex, in the frontal or in the occipital
lobe and directed to the tentory,[3]
[14] with extension and consequent rupture of the vessels due to shear forces[2]
[11]
[15] resulting in hemorrhages in the BG,[3] both the striking and counter-striking movements can develop this mechanical action.[16] The vessels associated with this phenomenon are the anterior choroidal artery and
the striated lenticular perforating arteries,[5]
[7]
[8] with the latter being associated with pediatric BGTH. The middle cerebral artery
(MCA) is associated with bleeding and infarction of the basal ganglia and the thalamus.[17] As the skull of children is elastic, the shear forces occur mildly in them compared
with adults.[6]
Bilateral lesions in the BG are associated with a low value on the GCS score due to
the connection of these structures to the ascending reticular activating system (ARDS).[11] The measure of remaining awake after TBI is related to bilateral atrophy of the
globus pallidus and putamen.[10]
Symptomatology
As the BG are the union of several parts of the brain's gray matter, the symptoms
manifest depending on the BG involved. When the internal capsule has a hematoma, the
associated symptom is motor deficit. Extrapyramidal symptoms appear when the substantia
nigra is damaged. Visual deficits and language and sensory disorders are associated
with the lateral geniculate bodies and the thalamus. When the ARDS has a hematoma,
the patient is unconscious.[7]
In their study, Moe et al.[11] demonstrated that patients with bilateral BG lesions and absence of other intracranial
lesions present low level of awareness at the accident site or at hospital admission.
Colquhoun et al.,[5] in a study conducted with 26 patients, showed the presence of a lucid interval in
nine patients, and the presence of focal neurological deficit was associated with
unilateral hematoma in the BG.
Diagnosis
The diagnosis is made through imaging exams. Computed tomography and magnetic resonance
imaging (MRI) show a hematoma with localization in the BG, associated with a skull
fracture,[13] and intraventricular and subarachnoid hematomas.[5] Diffuse axonal injury can be found in the imaging exams, being frequently associated
with a low GCS score.[2] Computed tomography can present a diffuse lesion of the cerebral white matter, present
in one third of patients with BGTH, often associated with increased intracranial pressure
and a poor prognosis.[18]
Treatment
The treatment of BGTH follows the protocol of intracranial hematomas, considering
the neurological status, mass effect, and high intracranial pressure.[5] Management can be achieved through conservative treatment, surgical drainage of
the hematoma, aspiration of the hematoma guided by ultrasound or stereotactic CT.[1]
[2] Surgical drainage is recommended for hematomas with a volume greater than 25 ml,
especially when associated with increased intracranial pressure.[7]
[14] In the present study, 13 patients were treated conservatively and 3 surgically,
aiming at draining bruises associated with BGTH lesions, two EDH and one SDH.
Complications
The poor prognosis of patients with BGTH[4] is related to the global characteristic of this brain lesion,[13] associated with the presence of intracranial hypertension,[5] presenting a poorer prognosis rate higher than other traumatic intracranial hemorrhage
types.[9] The factors associated with poor prognosis are age > 60 years, DAI, large volume
hematoma, extra-axial hematomas, abnormal pupillary and motor responses, severe TBI[14]
[16] and late hematoma increase.[2]
Zakharova et al.,[19] in a study with 278 patients, demonstrated that lesions located in the BG have a
prognosis of adverse outcomes such as vegetative state, severe neurological deficit,
and death. The high incidence of BG hematomas during autopsies demonstrates the clinical
course of death.[7]
[8] Mortality in pediatric patients varies between 14 and 33%.[6]
In the present case series, seven patients survived, three were in a good general
condition, and four had neurological sequelae such as dysphasia, motor deficit, convulsive
crises, and involuntary movements, and nine patients died.
Conclusion
Neurosurgeons' knowledge of BGTH is extremely important, including the symptoms related
to the affected areas, the diagnosis, and clinical or surgical management, since this
type of lesion is associated with a poor prognosis.