Complications following craniocerebral injuries include traumatic cerebrospinal fluid (CSF) leakage, post-traumatic hydrocephalus, skull defects, traumatic epilepsy, post-traumatic syndrome, hypothalamic injury after brain trauma, and psychiatric disorders following craniocerebral injuries.
Traumatic Cerebrospinal Fluid Leakage
This can be seen in the section on skull base fractures.
Post-Traumatic Hydrocephalus
The incidence of secondary hydrocephalus after craniocerebral injuries ranges from 10% to 30% and can be classified into acute and chronic types. Acute hydrocephalus typically results from blood clots obstructing the CSF circulation pathways (obstructive hydrocephalus) and presents with symptoms of worsening intracranial pressure or deepened consciousness disturbances. Chronic hydrocephalus often arises from subarachnoid hemorrhage following trauma, leading to impaired CSF absorption by arachnoid granulations (communicating hydrocephalus). It usually manifests 1–3 months after trauma with symptoms of increased intracranial pressure. Head CT or MRI scans reveal bilateral ventricular or entire ventricular system enlargement and periventricular edema surrounding the frontal horns, known as the "cap sign." Treatment typically involves ventriculoperitoneal shunt surgery.
Skull Defects
Skull defects after craniocerebral injuries are mostly caused by decompressive craniectomy performed after trauma, with direct trauma-induced skull defects being rare. Palpation may reveal pulsations of brain tissue in the defect area, with bulging and increased tension of the scalp over the defect during coughing, lying flat, or elevated intracranial pressure. Head CT or HRCT scans are used to evaluate the extent of the bone defect. Small defects covered by thick muscle tissue do not warrant surgery, whereas large defects require cranioplasty. The timing of surgery begins one month after the skull defect occurs. If scalp infection or high intracranial pressure leading to tension in the scalp over the defect is present, cranioplasty may be delayed.
Traumatic Epilepsy
Post-traumatic epilepsy is categorized into early-onset and late-onset forms. Early-onset epilepsy occurs during the acute phase of the brain injury, usually within the first week, and is often caused by brain contusion, intracranial hematoma, subarachnoid hemorrhage, depressed skull fractures, or acute brain edema. Late-onset epilepsy occurs after the acute phase, typically appearing 3 months to several years post-injury, and is associated with meningo-cerebral scars, ventricular deformities, intracranial infections, brain atrophy, or hydrocephalus. Diagnostic evaluations often include EEG, video EEG, MRI, and PET-CT. Traumatic epilepsy is primarily managed with medication, which can control seizures in most cases. Treatment generally requires continuous medication for over a year, with gradual dose reduction before discontinuation. Surgical resection of the epileptogenic focus can be considered for drug-resistant epilepsy, followed by adjunctive anti-epileptic drug therapy post-surgery.
Post-Traumatic Syndrome
Post-traumatic syndrome refers to a range of autonomic symptoms that appear months after the injury, including headache, dizziness, tinnitus, insomnia, memory decline, depression, and mood swings. Physical examinations typically do not reveal significant abnormalities, and head CT, MRI, and EEG findings are often unremarkable. Treatment primarily involves psychological and symptomatic management, including sedatives, analgesics for headaches, psychological counseling, and antidepressants.
Hypothalamic Injury After Brain Trauma
Hypothalamic injury after trauma is relatively rare and is often accompanied by other brain contusions or intracranial hematomas. It is caused by the intense displacement of brain tissue during the injury. Manifestations include somnolence, coma, hyperthermia or hypothermia, diabetes insipidus, gastric bleeding, slowed respiration, and neurogenic pulmonary edema. Head MRI is used for diagnosis. Treatment is similar to that of brain contusion and laceration, with additional symptomatic management.
Psychiatric Disorders Following Craniocerebral Injuries
Psychiatric disorders following trauma arise from brain tissue damage, individual personality traits, and psychosocial factors after the injury, with an incidence exceeding 25%. These disorders are classified into acute and chronic types. Acute psychiatric disorders typically involve symptoms such as agitation, insomnia, vivid dreaming, mood and behavioral disturbances, hallucinations, and delirium, which generally resolve within two weeks. Chronic psychiatric disorders are characterized by persistent symptoms such as difficulty concentrating, depression, chronic cognitive dysfunction, personality changes, or schizophrenia-like symptoms. Management includes psychological therapy, anti-anxiety or antidepressant medications, and behavioral therapy.