Introduction

Primary (direct) or secondary (indirect) traumatic injuries of brain structures localized within the posterior fossa (i.e., cerebellum and brainstem) are called ‘posterior fossa trauma’ (Fisher et al., 1958 Tsai et al., 1980).Primary traumatic injuries are commonly subdivided into open/closed head injuries, and intra-/extra-axial lesions. Open head injuries are characterized by opening of the subarachnoid space to the outside with liquorrhea, and are caused by penetrating injuries or by fractures. In closed head injuries the subarachnoid space remains intact. Intra-axial brain lesions lead to intraparenchymal damage, namely cerebellar or brainstem concussion and contusion, diffuse axonal injury due to shearing forces and delayed post-traumatic intracerebellar hematomas. Extra-axial injuries include epidural hematomas, subdural hematomas, and subarachnoid hemorrhages. Furthermore, vascular lesions may occur due to traumatic dissection of the vertebral arteries with subsequent infarction of the cerebellum and/or brainstem. Secondary traumatic brain lesions develop after the primary impact and are usually due to pathologic brain responses to the primary injury (e.g., brain edema, infection, elevated intracranial pressure, brain herniation) (Zimmerman, 1991 Keidel and Miller, 1996).

Despite advances in the understanding of the pathophysiology of primary and secondary brain injuries and in the management of patients with severe head trauma, posterior fossa trauma remains a life-threatening condition, which allows no delay in diagnosis and management. This chapter gives an overview of types, clinical and radiological presentation of posterior fossa trauma. The chapter also describes the pathophysiology and management of posterior fossa trauma. Special operative techniques are not described.

Introduction

Definitions

The term ‘ataxia’ (Greek, a- (= negative article) + taxi (= order), (‘lack of order’) is commonly used synonymously with incoordination (Dow & Moruzzi, 1958; Gilman et al., 1981; Timmann & Diener, 1998). Ataxia is the most important sign of cerebellar disease. Cerebellar ataxia is defined as lack of accuracy or coordination of movement which is not due to paresis, alteration in tone, loss of postural sense or the presence of involuntary movements (DeJong, 1979). Cerebellar ataxia relates to motor dysfunctions of the limbs, trunk, eyes, and bulbar musculature. Ataxia of gait refers to incoordination of walking, which might be so severe that the patient cannot walk (abasia). Postural ataxia refers to ataxia of stance and sitting and includes truncal ataxia.The patient may be unable to sit or stand without support (astasia). Limb ataxia refers to incoordination of limb movements and ataxia of speech to cerebellar dysarthia.

Cerebellar disease results in postural and limb tremor. There may be a rhythmic tremor of the body that can evolve into a severe titubation. Limb tremor occurs as a kinetic and to a lesser extent static tremor. Kinetic tremor occurs as an oscillatory movement when the subject initiates a movement of the limb or during the course of moving the limb. The tremor becomes more prominent as the moving limb approaches a target (intention tremor). Powerful, but brief involuntary movements at the beginning of the movement are due to intention myoclonus, not tremor, and occur in diseases involving the dentate nucleus or the superior cerebellar peduncle.

Neurological findings in cerebellar disease

Patients with cerebellar disorders walk with a wide-based, staggering gait, making it seem as if they were intoxicated by alcohol.