Cranioplasty
Barbara A. Wilson, Samira Kashinath Dhamapurkar, Anita Rose in Surviving Brain Damage After Assault, 2016
The decompressive craniectomy is often seen as a potentially life-saving procedure in the management of patients who have a medically intractable intracranial hypertension secondary to severe traumatic head injuries or following significant strokes (Aaribi et al., 2006). More recently, this procedure has also been used following subarachnoid haemorrhage, intracranial infection and inflammatory conditions (Ahmed et al., 2010; Baussart et al., 2006; Güresir et al., 2009). During the procedure, the surgeon temporarily removes a large segment of the skull in order to provide extra space into which the injured or oedematous brain can expand. This can be performed either unilaterally or bilaterally depending on the severity of the injury or swelling. This technique was first described by Harvey Cushing in 1905, and decompressive cranioectomies have been increasingly performed since that time even though the efficacy of such a procedure is still highly controversial. There is also similar controversy around the necessity of cranial reconstruction, a cranioplasty after such a procedure (Yang et al., 2003).
Overcoming the challenges of accurately assessing consciousness and communication in the context of pain assessment
Camille Chatelle, Steven Laureys in Assessing Pain and Communication in Disorders of Consciousness, 2015
Figure 4.2 shows command-following data over time to illustrate that the reliability of command-following changes gradually during recovery. The patient is a 32-year-old man who was injured in a fall of 20–30 feet. He suffered a seizure at the scene. On evaluation at the trauma center, he had a Glasgow Coma Score of five, and a CT scan revealed a right epidural hematoma with right to left shift, as well as multiple contusions. A craniectomy was performed, along with evacuation of the hematoma, but an early cranioplasty was performed six weeks post-injury and he was admitted to rehabilitation 10 weeks post-injury. On admission he was thought to occasionally touch his head or move his leg on command. Therefore, a dual-command protocol was begun in which he was randomly requested to “touch your head” or “move your leg.” Each trial was scored as “no response,” a head touch, or a leg movement. In general it was found that he made few errors but failed to respond at all on a substantial number of trials (see Figure 4.2 for a plot of his response rate [proportion of trials on which he responded]).
Neurovascular Photonics
Yu Chen, Babak Kateb in Neurophotonics and Brain Mapping, 2017
The first experimental use of lasers in neurosurgery was on animal models by Earle et al. (1965) and Fine et al. (1965). Pulsed-wave ruby laser was used, and a single high-energy pulse was applied to intact craniums of mice. The mice were immediately killed due to rapid expansion of the intracranial contents and subsequent cerebral herniation. Although herniation could be prevented by wide craniectomy in later studies, the destructive neural effect was intolerable, leading to wedge-shaped lesions and intracranial bleeding (Ryan et al., 2009). In 1966, Rosomoff and Carroll, for the first time, used the pulsed ruby laser on human glioma. Although there was an evidence of tumor necrosis, the thermal effects of the laser were difficult to control.
The therapeutic value of cranioplasty in individuals with brain injury
Published in Brain Injury, 2018
Neil Jasey, Irene Ward, Anthony Lequerica, Nancy D Chiaravalloti
Decompressive craniectomy is a surgical procedure in which a portion of the skull is removed, typically to relieve intracranial pressure in emergent situations in which few alternatives are available to ensure survival. After a variable period of time, the detached portion of the cranium or a synthetic prosthesis is reattached, known as cranioplasty surgery. Decompressive craniectomy has been performed across a number of neurologic conditions. Although more commonly performed after a traumatic brain injury, ischemic stroke or subarachnoid haemorrhage, decompressive craniectomy has also been performed following other brain-related conditions such as cerebral thrombus, encephalitis, subdural empyema, toxoplasmosis, demyelination, diabetic ketoacidosis, Reyes Syndrome and encephalopathy (1). Research articles have reported that decompressive craniectomy lowered the risk of death or severe disability following ischemic or traumatic brain injury (2–4). However, the long-term functional implications and the impact on rehabilitation of craniectomy and cranioplasty remain uninvestigated.
The incidence and treatment of seizures after cranioplasty: a systematic review and meta-analysis
Published in British Journal of Neurosurgery, 2018
As the application of decompressive craniectomy extends widely to severe traumatic brain injury and massive stroke, clinicians are expected to encounter more cases of cranioplasty. Despite the technically simple procedure, cranioplasty is associated with a high rate of complications. As different complications have specific incidences and treatment, separately reporting the complications is more informative. Seizures are common complications after cranioplasty, which complicates patients’ recovery and are significantly associated with poor outcomes.1,2 In the early years, cranioplasty was said to exert beneficial effect on the post-traumatic seizure.3,4 In contrast, recent studies found cranioplasty increased the risk of seizures. Many studies considered seizures as the most common complication after cranioplasty.5,6 The reported incidences of seizures vary greatly and the application of prophylactic antiepileptic drugs (AEDs) remains controversial. It is important to ascertain the accurate incidence of post-cranioplasty seizures to guide the preventive and therapeutic modalities. We conduct this systematic review to determine the pooled incidence of post-cranioplasty seizures and potential risk factors. Moreover, we clarify the effect of prophylactic AEDs on the post-cranioplasty seizures.
Improvement of cerebral blood perfusion in certain cerebral regions after cranioplasty could be monitored via tympanic membrane temperature changes
Published in Brain Injury, 2018
Ying Jiang, Yun-Kun Wang, Xiao-Lei Shi, Shen-Hao Wang, Yi-Ming Li, Jun-Yu Wang, Dan-Feng Zhang, Chao Ma, Ming-Kun Yu, Li-Jun Hou
Based on the previous two paragraphs, we believed that the cranioplasty could eliminate the negative impact of craniectomy on cerebral autoregulation and thus restore the cerebral perfusion. We hypothesized that the underlying physiology of the benefits of a reassembled skull is as follows. After craniectomy, a large cranial defect is left on the skull. This defect allows atmospheric pressure to be directly transmitted to the intracranial cavity, which results in an increased external pressure on the local cortex and a pressure gradient on both cerebral hemispheres (31,32). Cerebral autoregulation, including both the artery (7) and vein system (31), is compromised in the presence of this extra pressure. Under such circumstances, misery perfusion is expected in both the decompressed and contralateral hemispheres. After cranioplasty, the atmospheric pressure is eliminated on both hemispheres, with a resultant increase in cerebral perfusion (6,23–26) and vascular reserve capacity (7). These changes indicate the restoration of cerebral autoregulation by cranioplasty. In the current study, we found that the ACA and MCA perfused cerebral in different patterns after cranioplasty, which also supports the phenomenon of cerebral autoregulation recovery. Additionally, one study reported disproportionately large change (∼30–50% increase) in CBF is required to support a relatively small change (∼5%) in the O2 metabolic rate (33). Thus, we are really surprised to see that MCA mainly upregulates the MTT in its perfused regions, which is a more sufficient strategy to increase perfusion amount.
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