Patients may develop late complications.Delayed onset cerebellar syndromerefers to the appearance of cerebel- lar deficits between 3 weeks and 2 years after trauma (Louis et al., 1996).The syndrome may take a pro- gressive course, with a worsening over a few months.
The pathogenesis might be a hypersensitivity of post- synaptic sites within the cerebellar outflow tracts (see Chapter1). A proportion of patients exhibit a so-called
“delayed-onset intention tremor.” In others, tremor is present at rest, during postural tasks, and during movement (midbrain tremor). Children with a history of moderate to severe traumatic brain injury (Glas- gow Coma Scale raging from 3 to 11) due to a vehicle, bicycle, or pedestrian–vehicle crash develop cerebellar atrophy of the white matter as demonstrated by quanti- tative MRI performed at a mean post-injury interval of 3.1±2.4 years (Spanos et al.,2007). Loss of cerebellar gray matter has been documented (Gale et al.,2005).
Autopsy studies confirm a loss of Purkinje neurons and activation of microglia (Matschke et al., 2007).
Inflammation, axonal lesions, and excitotoxic mecha- nisms might contribute to delayed neuronal loss. Deep brain stimulation of the Vim nucleus can improve post-traumatic cerebellar tremor in adults. However, kinetic tremor is more difficult to treat than rest or pos- tural tremor, and proximal tremor tends to be refrac- tory, although there are exceptions (Deuschl & Bain, 2002).
Olivary hypertrophymay be associated with palatal myoclonus (see also Chapter 3), as a consequence of a lesion of the Guillain-Mollaret triangle. Other involuntary movements may be associated, such as myoclonias of the neck or the shoulder. Cerebellar symptoms are contralateral to the site of hypertrophy when this latter develops unilaterally. Olivary hyper- trophy develops several months to several years after the trauma. Brain MRI shows abnormal signals in the inferior olive (Birbamer et al.,1994).Figure 14.7illus- trates an example. Lesions need to be distinguished from vascular, infectious, inflammatory, or neoplastic
causes.
151
Table 14.3 Results of imaging studies in posterior fossa trauma
Lesion CT scan MRI
Cerebellar contusion Ill-defined hypodense area (edema) Punctuate hyperdense areas (bleeding)
Note: possible bone fracture and often swelling of soft tissues
T1-weighted images: from hypointense (early stage) to hyperintense area (later stage) T2-weighted images: hyperintense area (edema)
Cerebellar hematoma Hyperdense area, possible mass effect with hydrocephalus
Possible ring enhancement surrounding the hematoma Subarachnoid
hemorrhage Hyperdense fluid in the cisterns, in the sulci, around the falx of cerebellum, in ventricles
Diffuse axonal injury Diffuse hypodensity (swelling)
Possible mass effect Multiple areas of increased signal intensity on T2-weighted images
Epidural hematoma Hyperdense lesion, with a biconvex shape
Mass effect is common T1-weighted images: isointense mass
T2-weighted images: hypointense mass Subdural hematoma Hyperdense lesion, with a concavo/convex shape
Often unilateral in adults and bilateral in children T1-weighted images: hypo/isointense on the top and hyperintense on the bottom
(“hematocrit-like effect”)
T2-weighted images: hyperintense/isointense on the top and hypointense on the bottom Dissection of vessels Hypodense area (infarction) Intramural hematoma, vessel occlusion,
pseudoaneurysma aMay be demonstrated by MRA.
A B
Figure 14.3 Bilateral subdural hematoma of the posterior fossa. (A) T1-weighted axial MRI shows fluid levels (“hematocrit effect”) due to sedimentation of erythrocytes (arrows). Asterisks corresponds to serum. (B) T2-weighted image showing a dark aspect of the hematoma (arrows). With permission from: Maschke et al.,2002.
A B
C
Figure 14.4 Epidural hematoma of the posterior fossa. (A) (bone window) Triangles indicate a fracture of the right temporal bone extending to the sulcus of the sigmoid sinus. (B, C) Biconvex hematoma extending above the tentorium cerebella. With permission from: Maschke et al., 2002.
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Chapter 14 – Trauma of the posterior fossa
A B
Figure 14.5 Dissection of the vertebral artery. (A) Infarction in the territory of the PICA (arrows) on axial MRI. (B) Angiography shows an arterial occlusion of the vertebral artery (arrow). From: Maschke et al.,2002. With permission.
Figure 14.6 (A) Relative hypermetabolism of the cerebellar vermis and pons in a patient with post-anoxic coma. (B) Control case. From: Lupi et al.,2007. With permission. (Seecolor section.)
154
Table 14.4. Management of posterior fossa trauma Acute phase
Cautious mobilization of patients
Monitoring and management of vital functions (stabilization of vital parameters)
Immediate brain imaging (CT or MRI)
Monitoring of intra-cranial pressure in severe head injury Increased intra-cranial pressure
Hyperventilation
Administration of osmotic agents (mannitol), diuretics, barbiturates
Drainage in case of obstructive hydrocephalus Surgical decompression in case of severe edema Management of space-occupying lesions
Surgical evacuation of hematoma (epidural, subdural) Dissection
Anticoagulation (intravenous heparin, followed by warfarin)
Chronic phase
Management of tremor (drugs, Vim stimulation, Botulinum toxin)
Rehabilitation Speech rehabilitation Physical therapy Assistive devices
Crossed atrophy of the cerebellumdevelops several months or years after a traumatic cerebral lesion, either by anterograde degeneration of the corticopontocere- bellar tract or by retrograde trans-synaptic degen- eration of the cerebello-rubrothalamic tract (Tien &
Ashdown,1992).Superficial siderosis in discussed in Chapter13.
Mood disorders and neuropsychological deficits developing several months to a year after trauma of the posterior fossa may occur. There is an associa- tion between cerebellar lesions and deficits in visual recognition memory, dyscalculia, and IQ in chil- dren after severe traumatic brain injury (Braga et al., 2007).
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