Traumatic Brain injury	91

have no other accompanying brain injuries and if the hematoma has been removed early enough.

Note: when an epidural hematoma is suspected, plain radiographs of the skull and MRI are both contraindicated. The former might reveal a fracture, but cannot reveal the hematoma; the latter will show the hematoma, but takes longer than CT, and time is of the essence.

Subdural hematomas can be acute, subacute, or chronic. The blood collection lies between the dura mater and the arachnoid and comes about because of a tear in a bridging vein.

Acute subdural hematoma is usually a component of severe traumatic brain injury with extensive intraparenchymal contusional hemorrhages. Clinical examination alone does not enable a clear-cut distinction between subdural and epidural hematomas: subdural hematoma, too, is characterized by a rapidly progressive decline of consciousness, ipsilateral pupillary dilatation, and contralateral hemiparesis. The diagnosis is established by CT: a subdural hematoma is typically seen as a hyperdense or isodense area (depending on the time elapsed since the traumatic event), either crescent shaped or closely applied to the skull; unlike an epidural hematoma, a subdural hematoma is poorly demarcated from the underlying brain tissue. Subdural hematomas, too, are treated by immediate neurosurgical evacuation.

Chronic subdural hematoma may arise in the aftermath of a mild traumatic brain injury or even after a relatively trivial blow to the head, of which the patient may no longer have any recollection. A few weeks or (rarely) months after the causative event, the patient begins to suffer from increasingly severe headache, fluctuating disturbances of consciousness, confusion, and ultimately progressive somnolence. Hemiparesis, if present, is usually mild and signs of intracranial hypertension are usually absent. The diagnosis is established by CT or MRI. The treatment is by neurosurgical evacuation through one or two burr holes (this is a relatively brief and uncomplicated procedure and can be performed under local anesthesia in cooperative patients). Therapeutic anticoagulation is a risk factor for the development of a chronic subdural hematoma.

Complications of Traumatic Brain Injury

Early Complications

Early posttraumatic infection. Any open or penetrating brain injury (e. g., depressed skull fractures, gunshot wounds) provides a route of access for bacterial contamination of the meningeal spaces and the brain. Early posttraumatic meningitis, subdural empyema, cerebritis, or a brain abscess may appear a few days or weeks after the traumatic event.

Later Complications

Late infection. A skull base fracture associated with a dural tear may create a cerebrospinal fluid fistula, manifesting clinically as leakage of clear fluid out the

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nose or ear (CSF rhinoor otorrhea) or into the pharynx. Leaking CSF fistulae are sometimes accompanied by orthostatic headache due to intracranial hypotension. If the fistula remains undiscovered or untreated, it can serve as a portal for bacterial infection. The patient may present with meningitis and/or a brain abscess, perhaps years after the initial trauma. The presence and exact location of a CSF fistula can be demonstrated by isotope cisternography (Fig. 4.12, p. 53); other useful studies include MRI and thin-section CT, which may reveal a bony defect or fracture. CSF fistulae should be surgically repaired.

Posttraumatic neurological deficits. The commonest cranial nerve deficit after traumatic brain injury is anosmia (p. 180), which is permanent in two-thirds of patients, followed by optic nerve injuries and palsies of the nerves to the eye muscles. Optic nerve dysfunction only rarely improves, but palsies of cranial nerves III, IV, and VI usually resolve in two to three months. Fractures of the petrous pyramid(s) may cause facial nerve palsy as well as deafness, due to injury either to the vestibulocochlear nerve or to the cochlea itself; when caused by a transverse fracture, deafness is usually permanent. A fracture extending into the jugular foramen may cause a combined palsy of the glossopharyngeal, vagus, and accessory nerves (Siebenmann syndrome). Focal brain lesions cause deficits according to their localization. Diencephalic lesions often cause diabetes insipidus. Spasticity may be unior bilateral. Cerebellar lesions are characterized by ataxia, which does not always resolve.

Posttraumatic epilepsy is seen within two years in 80 % of the patients who develop it, but it can also arise many years after the initial trauma in rare cases. The seizures may be focal, secondarily generalized, or primarily generalized (cf. p. 164).

Neuropsychological deficits and personality changes.

Posttraumatic neuropsychological deficits (variously designated focal organic brain syndrome, psycho-or- ganic syndrome, or posttraumatic encephalopathy) and personality changes are often the most disabling sequelae of traumatic brain injury for the patient and his or her family. The severity of these problems is positively correlated with the length of the initial loss of consciousness and with the duration of retrograde and anterograde amnesia around the time of the injury. Both shortand long-term memory are impaired and the attention span is shorter than normal. The patient has difficulty coping with complex tasks and situations and is easily fatigued. Impatience, irritability, diminished initiative, poor concentration, and lack of interest ranging to apathy characterize the patient’s behavior. The adverse psychosocial effects in personal and professional life are often very serious.

Rarer posttraumatic phenomena include a persistent Lhermitte sign (p. 157) or malresorptive hydrocephalus.

Malresorptive hydrocephalus most commonly arises after a traumatic subarachnoid hemorrhage and consists of an impairment of CSF flow and resorption due to adhesions of the arachnoid and of the arachnoid granulations. It can also arise in the aftermath of aneurysmal

Mumenthaler / Mattle, Fundamentals of Neurology © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.

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Diseases of the Brain and Meninges