Introduction

Acute traumatic subdural hematoma (ASDH) of the posterior cranial fossa is a very rare clinical event. The outcome is poor and the overall mortality rate is high [1, 2]. We report an unusual case of ASDH of the posterior fossa followed by mutism, which is a well-documented complication of posterior fossa tumor resection in children [3].

Case report

A 7-year-old, right-handed boy was involved in a road traffic accident. Immediately after admission, he suffered a generalized convulsion and became comatose. The pupils were isocoric, and the light reflex was prompt. A computed tomography scan revealed an ASDH of the posterior fossa, a traumatic subarachnoid hemorrhage (SAH) in the left sylvian cistern, and distortion of the brain stem (Fig. 1). The mesencephalic cisterns were obliterated and the fourth ventricle was compressed and deviated laterally, but acute hydrocephalus was not seen. Removal of the ASDH, which was commenced 1.5 h after injury, was performed by standard suboccipital craniotomy, and was completed 3.5 h after injury. The bleeding point was the superficial cerebellar vessels. The vermis was not incised. After extubation, which took place 3 days after surgery, the patient rapidly recovered consciousness, his eyes opened, and although he did not speak, he was able to follow commands. He began to utter 14 days after the injury, and to speak only in short sentences 1 day later. Subsequently, the patient’s mutism improved daily, and his speech became normal 39 days after injury. Magnetic resonance imaging 27 days after injury revealed a post-contusional change in the right cerebellum and an ischemic lesion in the pons (Fig. 2). The patient was discharged 74 days after injury with mild ataxia, without cranial nerve palsy, and with a full score on the Barthel index [4].

Fig. 1
figure 1

Computed tomography scan at admission. Acute subdural hematoma (arrow) of the posterior fossa and a traumatic subarachnoid hemorrhage were observed. The brain stem was distorted, but hydrocephalus was not seen

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Fig. 2
figure 2

Magnetic resonance image 27 days after injury. A post-contusional change in the cerebellum (white arrow) and an ischemic lesion (black arrow) in the pons are visible

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Discussion

In this case, surgery was performed successfully very early after the injury. As recommended in the literature [1], immediate hematoma removal is the only therapy for patients with ASDH of the posterior fossa.

Mutism is defined as an inability to produce verbal output in a cognitively alert patient, and may be due to damage to the Broca area, lesions in the supplementary motor cortex, dysfunction of the mesencephalic reticular formation, bilateral hemispherical lesions and thalamotomy [8, 11]. Mutism is usually seen after resection of a posterior fossa tumor with vermal incision (i.e., cerebellar mutism). Cerebrovascular events such as vermian arteriovenous malformation, a spontaneous vermian [5] or hemispheric hemorrhage [6, 7], midbrain or pontine cavernous malformation [8], and embolic occlusion of the basilar artery [9] are also reported to be causes of mutism. Miyakita et al. [10] reported an infarction of the midbrain down to the upper pons caused by a tracheal injury. However, reports of mutism due to head injury are scarce. Turgut [11] reviewed the literature and found reports of 93 patients with mutism. Of these 93 cases, traumatic injury was responsible for only one case. Yokota et al. [12] reported a case of traumatic injury of the cerebellar hemisphere in which mutism occurred. There are so far no reports of mutism after ASDH of the posterior fossa. In the present case, even after the patient recovered consciousness and became cognitively alert, he could not speak, and it took 39 days until the patient’s speech became normal. We believe that his mutism was caused by severe posterior fossa ASDH, although it is actually difficult to localize the anatomical substrate responsible for his mutism specifically, as discussed below.

Recently, Wang et al. [8] reported a case of midbrain cavernous malformation, and discussed in detail the pathogenesis of “cerebellar” mutism from an anatomical perspective. They concluded that rather than the cerebellar lesion per se, it is the connections between the dentate nucleus, the thalamus (dentatothalamic tracts), and the supplementary motor area that are involved. The efferent fibers from the dentate nucleus project through the superior cerebellar peduncle to the contralateral red nucleus, the ventrolateral nucleus of thalamus, and the reticular formation. The fibers from the thalamus project to the cerebral cortex (supplementary motor area). From the cortex, there are fibers projecting to the pons and the cerebellum (tractus corticopontinus cerebellaris). Thus, the circuits are formed between the dentate nucleus, red nucleus, thalamus, cerebral cortex, and pons. In the present case, the right cerebellar hemisphere, including the dentate nucleus, was severely compressed and the brain stem was distorted, as evidenced by the observation of pontine infarction. Although acute hydrocephalus was not present, the occurrence of generalized seizure at admission may implicate acute dysfunction of the cerebral cortex. Furthermore, traumatic SAH seen in the left sylvian cistern at admission may suggest that the Broca area, which is situated in close proximity to this area, is involved. Although any lesions of these structures (i.e., dentate nucleus, red nucleus, thalamus, cerebral cortex, and pons) are able to cause mutism, it may safely be said that all these pathological conditions were primarily caused by the severe ASDH of the posterior fossa. At any rate, the transient nature of this syndrome, which was also observed in the present case, suggests that the cause of the mutism is trauma-related edema and/or transient ischemia of these structures.