Category Archives: Neurotrauma

Update: Chronic traumatic encephalopathy in American football players

There is tremendous media attention regarding chronic traumatic encephalopathy (CTE), primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathology 1).

Physicians in clinical practice are likely to face an increasing number of retired football players seeking evaluation for chronic neurobehavioral symptoms. Guidelines for the evaluation and treatment of these patients are sparse. Clinical criteria for a diagnosis of CTE are under development. The contribution of CTE vs other neuropathologies to neurobehavioral symptoms in these players remains unclear.

Gardner et al. describe the experience in evaluating and treating a series of 14 self-referred symptomatic players. The aim is to raise awareness in the neurology community regarding the different clinical phenotypes, idiosyncratic but potentially treatable symptoms, and the spectrum of underlying neuropathologies in these players 2).

Altered Corpus Callosum White Matter Microstructure

Forty retired National Football League (NFL) players, ages 40-65, were matched by age and divided into two groups based on their age of first exposure (AFE) to tackle football: before age 12 or at age 12 or older. Participants underwent DTI on a 3 Tesla Siemens (TIM-Verio) magnet. The whole CC and five subregions were defined and seeded using deterministic tractography. Dependent measures were fractional anisotropy (FA), trace, axial diffusivity and radial diffusivity. Results showed that former NFL players in the AFE <12 group had significantly lower FA in anterior three CC regions and higher radial diffusivity in the most anterior CC region than those in the AFE ≥12 group. 3).

Prevention

Findings suggest that regulation of practice equipment could be a fair and effective way to substantially reduce subconcussive head impact in thousands of collegiate football players 4).

Case series

2017

Case series of 202 football players whose brains were donated for research. Neuropathological evaluations and retrospective telephone clinical assessments (including head trauma history) with informants were performed blinded. Online questionnaires ascertained athletic and military history.

Neuropathological diagnoses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomized into mild [stages I and II] and severe [stages III and IV]); informant-reported athletic history and, for players who died in 2014 or later, clinical presentation, including behavior, mood, and cognitive symptoms and dementia.

Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre-high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology. Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia.

In a convenience sample of deceased football players who donated their brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior participation in football 5).

1)

Riley DO, Robbins CA, Cantu RC, Stern RA. Chronic traumatic encephalopathy: Contributions from the Boston University Center for the Study of Traumatic Encephalopathy. Brain Inj. 2015;29(2):154-63. doi: 10.3109/02699052.2014.965215. PubMed PMID: 25587744.
2)

Gardner RC, Possin KL, Hess CP, Huang EJ, Grinberg LT, Nolan AL, Cohn-Sheehy BI, Ghosh PM, Lanata S, Merrilees J, Kramer JH, Berger MS, Miller BL, Yaffe K, Rabinovici GD. Evaluating and treating neurobehavioral symptoms in professional American football players: Lessons from a case series. Neurol Clin Pract. 2015 Aug;5(4):285-295. PubMed PMID: 26336629.
3)

Stamm JM, Koerte IK, Muehlmann M, Pasternak O, Bourlas AP, Baugh CM, Giwerc MY, Zhu A, Coleman MJ, Fritts NG, Martin B, Chaisson C, McClean MD, Lin AP, Cantu RC, Tripodis Y, Stern R, Shenton ME. Age at First Exposure to Football is Associated with Altered Corpus Callosum White Matter Microstructure in Former Professional Football Players. J Neurotrauma. 2015 Jul 22. [Epub ahead of print] PubMed PMID: 26200068.
4)

Reynolds BB, Patrie J, Henry EJ, Goodkin HP, Broshek DK, Wintermark M, Druzgal TJ. Practice type effects on head impact in collegiate football. J Neurosurg. 2015 Aug 4:1-10. [Epub ahead of print] PubMed PMID: 26238972.
5)

Mez J, Daneshvar DH, Kiernan PT, Abdolmohammadi B, Alvarez VE, Huber BR, Alosco ML, Solomon TM, Nowinski CJ, McHale L, Cormier KA, Kubilus CA, Martin BM, Murphy L, Baugh CM, Montenigro PH, Chaisson CE, Tripodis Y, Kowall NW, Weuve J, McClean MD, Cantu RC, Goldstein LE, Katz DI, Stern RA, Stein TD, McKee AC. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017 Jul 25;318(4):360-370. doi: 10.1001/jama.2017.8334. PubMed PMID: 28742910.

Update: Posttraumatic epilepsy

Traumatic brain injury (TBI) is one of the most common causes of acquired epilepsy, and posttraumatic epilepsy (PTE) results in significant somatic and psychosocial morbidity.

The incidence of early post-traumatic seizures after civilian traumatic brain injury ranges 4-25%.

The true incidence of PTE in children is still uncertain, because most research has been based primarily on adults.

PTE in a pediatric population with mild traumatic brain injury (MTBI), was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population 1).

Risk

The risk of developing PTE relates directly to TBI severity, but the latency to first seizure can be decades after the inciting trauma. Given this “silent period,” much work has focused on identification of molecular and radiographic biomarkers for risk stratification and on development of therapies to prevent epileptogenesis.

Research suggests that there are reciprocal relationships between mental health (MH) disorders and epilepsy risk.

Data suggest that PTE is associated with mental health (MH) outcomes 2years after TBI, findings whose significance may reflect reciprocal, biological, psychological, and/or experiential factors contributing to and resulting from both PTE and MH status post-TBI. Future work should consider temporal and reciprocal relationships between PTE and MH as well as if/how treatment of each condition influences biosusceptibility to the other condition 2).

Treatment

The control of early post-traumatic seizure is mandatory because these acute insults may add secondary damage to the already damaged brain with poor outcome. Prophylactic use of antiepileptic drugs have been found to be have variable efficacy against early post-traumatic seizures.

Based on current studies, however, anticonvulsants have been shown to reduce early PTE occurring within the first 7 days, but little to no benefits have been shown in late PTS occurring after 7 days 3).

Clinical management requires vigilant neurologic surveillance and recognition of the heterogeneous endophenotypes associated with PTE.

Appropriate treatment of patients who have or are at risk for seizures varies as a function of time after TBI, and the clinician’s armamentarium includes an ever-expanding diversity of pharmacological and surgical options.


The lack of evidence on which antiepileptic drug to use in PTE is surprising given the number of patients prescribed an antiepileptic drug therapy for TBI. On the basis of currently available Level III evidence, patients treated with either levetiracetam or phenytoin have similar incidences of early seizures after TBI 4).

There is no statistically significant difference in the efficacy of Phenytoin and Levetiracetam in prophylaxis of early posttraumatic seizures in cases of moderate to severe traumatic brain injury 5).


Most recently, neuromodulation with implantable devices has emerged as a promising therapeutic strategy for some patients with refractory PTE 6).

Systematic review

During June and July 2015, a systematic literature search was performed that identified 6097 articles. Of these, 7 met inclusion criteria. A random-effects meta-analysis was performed. A total of 1186 patients were included. The rate of seizure was 35 of 654 (5.4%) in the levetiracetam cohort and 18 of 532 (3.4%) in the phenytoin cohort. The meta-analysis revealed no change in the rate of early PTS with levetiracetam compared with phenytoin (relative risk, 1.02; 95% confidence interval, 0.53-1.95; P = .96).

The lack of evidence on which antiepileptic drug to use in PTS is surprising given the number of patients prescribed an antiepileptic drug therapy for TBI. On the basis of currently available Level III evidence, patients treated with either levetiracetam or phenytoin have similar incidences of early seizures after TBI 7)

Case series

2016

In a retrospective multicenter cohort study including 5 regional pediatric trauma centers affiliated with academic medical centers, the authors examined data from 236 children (age < 18 years) with severe traumatic brain injury (TBI) (admission Glasgow Coma Scale score ≤ 8, ICD-9 diagnosis codes of 800.0-801.9, 803.0-804.9, 850.0-854.1, 959.01, 950.1-950.3, 995.55, maximum head Abbreviated Injury Scale score ≥ 3) who received tracheal intubation for ≥ 48 hours in the ICU between 2007 and 2011.

Of 236 patients, 187 (79%) received seizure prophylaxis. In 2 of the 5 centers, 100% of the patients received seizure prophylaxis medication. Use of seizure prophylaxis was associated with younger patient age (p < 0.001), inflicted TBI (p < 0.001), subdural hematoma (p = 0.02), cerebral infarction (p < 0.001), and use of electroencephalography (p = 0.023), but not higher Injury Severity Score. In 63% cases in which seizure prophylaxis was used, the patients were given the first medication within 24 hours of injury, and 50% of the patients received the first dose in the prehospital or emergency department setting. Initial seizure prophylaxis was most commonly with fosphenytoin (47%), followed by phenytoin (40%).

While fosphenytoin was the most commonly used medication for seizure prophylaxis, there was large variation within and between trauma centers with respect to timing and choice of seizure prophylaxis in severe pediatric TBI. The heterogeneity in seizure prophylaxis use may explain the previously observed lack of relationship between seizure prophylaxis and outcomes 8).

1)

Keret A, Bennett-Back O, Rosenthal G, Gilboa T, Shweiki M, Shoshan Y, Benifla M. Posttraumatic epilepsy: long-term follow-up of children with mild traumatic brain injury. J Neurosurg Pediatr. 2017 Jul;20(1):64-70. doi: 10.3171/2017.2.PEDS16585. Epub 2017 May 5. PubMed PMID: 28474982.

2)

Juengst SB, Wagner AK, Ritter AC, Szaflarski JP, Walker WC, Zafonte RD, Brown AW, Hammond FM, Pugh MJ, Shea T, Krellman JW, Bushnik T, Arenth PM. Post-traumatic epilepsy associations with mental health outcomes in the first two years after moderate to severe TBI: A TBI Model Systems analysis. Epilepsy Behav. 2017 Jun 25;73:240-246. doi: 10.1016/j.yebeh.2017.06.001. [Epub ahead of print] PubMed PMID: 28658654.

3)

Kirmani BF, Robinson DM, Fonkem E, Graf K, Huang JH. Role of Anticonvulsants in the Management of Posttraumatic Epilepsy. Front Neurol. 2016 Mar 22;7:32. eCollection 2016. Review. PubMed PMID: 27047441.

4)

Khan NR, VanLandingham MA, Fierst TM, Hymel C, Hoes K, Evans LT, Mayer R, Barker F, Klimo P Jr. Should Levetiracetam or Phenytoin Be Used for Posttraumatic Seizure Prophylaxis? A Systematic Review of the Literature and Meta-analysis. Neurosurgery. 2016 Sep 30. PubMed PMID: 27749510.

5)

Khan SA, Bhatti SN, Khan AA, Khan Afridi EA, Muhammad G, Gul N, Zadran KK, Alam S, Aurangzeb A. Comparison Of Efficacy Of Phenytoin And Levetiracetam For Prevention Of Early Post Traumatic Seizures. J Ayub Med Coll Abbottabad. 2016 Jul-Sep;28(3):455-460. PubMed PMID: 28712212.

6)

Rao VR, Parko KL. Clinical Approach to Posttraumatic Epilepsy. Semin Neurol. 2015 Feb;35(1):57-63. Epub 2015 Feb 25. PubMed PMID: 25714868.

7)

Khan NR, VanLandingham MA, Fierst TM, Hymel C, Hoes K, Evans LT, Mayer R, Barker F, Klimo P Jr. Should Levetiracetam or Phenytoin Be Used for Posttraumatic Seizure Prophylaxis? A Systematic Review of the Literature and Meta-analysis. Neurosurgery. 2016 Dec;79(6):775-782. PubMed PMID: 27749510.

8)

Ostahowski PJ, Kannan N, Wainwright MS, Qiu Q, Mink RB, Groner JI, Bell MJ, Giza CC, Zatzick DF, Ellenbogen RG, Boyle LN, Mitchell PH, Vavilala MS; PEGASUS (Pediatric Guideline Adherence and Outcomes) Study.. Variation in seizure prophylaxis in severe pediatric traumatic brain injury. J Neurosurg Pediatr. 2016 Oct;18(4):499-506. PubMed PMID: 27258588.

Update: Bilateral chronic subdural hematoma

Data on bilateral chronic subdural hematomas (CSHs) are scant 1) , including information on the frequency of symptoms, response to various treatments, and postoperative complications, compared with data on unilateral CSH. Bilateral CSHs constitute a fair portion of CSHs, especially in patients older than 75 years and in those with coagulopathy.

Clinical features

The presenting symptoms are those of raised intracranial pressure and mass effect.

The frequency of focal neurological deficits was found to be lesser in patients with bilateral CSDH, and it may confound the diagnosis and delay treatment 2).

Diagnosis

Computed tomography

Bilateral hematomas may lead to medial compression of both ventricles resulting in a narrow, slit-like elongated ventricle (the anterior horns sharply pointed and approaching one another so called ‘squeezed ventricle,’ ‘hare’s ears sign, or ‘rabbit’s ears’) 3) 4)5) 6).

see also Bilateral isodense chronic subdural hematoma

Magnetic resonance imaging

Magnetic resonance imaging is a more sensitive modality.

Differential diagnosis

If the lesion is placed more anteriorly and medially, hyperdense in intensity and enclosed in thick capsule, it may look biconvex in shape and can mimic extradural hematoma. This location of the lesion will also displace the frontal horns of the lateral ventricles laterally than medially, as in the present case. To avoid this confusion, if available, magnetic resonance imaging (MRI) would be better than CT in identifying these lesions 7) 8) 9) 10) 11).

Treatment

Occasionally patients with bilateral CSDH undergo unilateral surgery because the contralateral hematoma is deemed to be asymptomatic, and in some of these patients the contralateral hematoma may subsequently enlarge, requiring additional surgery.

Treatment of bilateral CSHs presents its own unique set of problems. New hemorrhage on the contralateral side and shift of midline structures are concerns and can be avoided by simultaneous bilateral decompression 12) 13). and significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 14).

To prevent neurological deterioration resulting from the thicker hematomas, early surgical decompression for bilateral CSDH should be implemented 15).

Outcome

Mixed high and low intensity in T2WI or low intensity in T1WI is the most predictable factor to show rapid aggravation 16).

Clinicians must be aware of the higher recurrent rate of bilateral CSDH after burr hole craniostomy 17).

Case series

2017

Two hundred ninety-one patients with bCSDH were identified, and 264 of them underwent unilateral (136 patients) or bilateral (128 patients) surgery. The overall retreatment rate was 21.6% (57 of 264 patients). Cases treated with unilateral surgery had twice the risk of retreatment compared with cases undergoing bilateral surgery (28.7% vs 14.1%, respectively, p = 0.002). In accordance with previous studies, the data also showed that a separated hematoma density and the absence of postoperative drainage were independent predictors of retreatment.

In bCSDHs bilateral surgical intervention significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 18).


Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.

The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).

The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 19).

2013

Huang et al., identified 25 of 98 CSDH (25.51%). The patients with bilateral lesions had a lower incidence of hemiparesis than those having unilateral lesions (p = 0.004). Analysis of the neuro-images revealed significant differences in the presence of a midline shift (p = 0.001) and thickness of the hematoma (p < 0.001).

The mean Markwalder grading score at admission was 1.89 ± 0.66 and 1.64 ± 0.49 in the unilateral and bilateral hematoma groups, respectively (p = 0.010). After a minimum follow-up period of 6 months, the mean Glasgow Outcome Scale was not significantly different (p = 0.060). The recurrence rate of up to 28.00% observed for the bilateral disease was found to be higher than 9.59% observed for the unilateral disease (p = 0.042) 20).

Case reports

2017

A 72-year-old man with bilateral chronic subdural hematomas was admitted and treated using a YL-1 type hematoma aspiration needle. The treatment was complicated by hemorrhage of the basal ganglia and brainstem. This patient had no history of hypertension. Chen et al evaluated the relevant literature to analyze the causes of cerebral hemorrhage in similar patients.

This case report illustrates that the stability of the intracranial pressure should be closely monitored during the surgical treatment of chronic subdural hematomas, and large fluctuations in the cerebral perfusion pressure should be avoided during the operation. They also propose improvements in the technical details of the operative treatment of chronic subdural hematomas 21).


Calcified chronic subdural hematomas are an occurrence rarely seen in neurosurgical clinical practice. And when they occur bilaterally, the radiologic image they present is fascinating, as is the clinical presentation, but their management may be challenging. They have been reported to present with a multitude of neurologic deficits but never with diabetes insipidus, which is described by Siddiqui et al.

Due to the rarity of this pathology, the management protocol is not well defined, though there have been quite a few papers on this condition. This review article gathers information published over the years on this rare entity to suggest a treatment protocol 22).

2006

An 81-year-old man suffered blunt trauma to his chest resulting from a road traffic accident. On admission a chest X-ray showed multiple rib fractures but a computerized tomography scan of the head ruled out any post-traumatic lesion. He had a background diagnosis of mild Alzheimer’s dementia for which he was being treated with galantamine. He lived a reasonably independent life with his wife and was driving the car himself when the accident occurred. After a fortnight he was discharged from hospital.

Two months later he developed progressive deterioration in mobility. His wife noted an increasing level of forgetfulness and intermittent episodes of confusion. His general practitioner noted a shuffling gait and rigidity affecting lower limbs and made a working diagnosis of parkinsonism. A trial of Madopar (Levodopa and benserazide: 62.5 mg three times a day for 2 weeks) was given by the GP but this failed to improve the situation and he became virtually bed-bound. He was referred back to the hospital for further investigation.

On admission he was confused and marked rigidity affecting upper and lower limbs was detected. No resting tremor was noted but gait could not be tested, as he was unable to get out of bed. In view of the clinical presentation a computerized tomography scan of the head was repeated which showed bilateral fronto-parietal chronic subdural haematoma (Figure 1a,b). He was referred to the regional neurosurgical centre where he underwent bilateral burrhole drainage. Postoperative recovery was unremarkable and on examination there was complete resolution of previous rigidity affecting upper and lower limbs. He was able to converse normally with his wife and began walking with the aid of a stick by third postoperative day. A week later he was discharged from the hospital having regained his previous level of mobility and independence with activities of daily living 23).

1)

Schaller B, Radziwill AJ, Wasner M, Gratzl O, Steck AJ. [Intermittent paraparesis as manifestation of a bilateral chronic subdural hematoma]. Schweiz Med Wochenschr. 1999 Jul 27;129(29-30):1067-72. German. PubMed PMID: 10464909.
2) , 15) , 17) , 20)

Huang YH, Yang KY, Lee TC, Liao CC. Bilateral chronic subdural hematoma: what is the clinical significance? Int J Surg. 2013;11(7):544-8. doi: 10.1016/j.ijsu.2013.05.007. Epub 2013 May 24. PubMed PMID: 23707986.
3)

Marcu H, Becker H. Computed-tomography of bilateral isodense chronic subdural hematomas. Neuroradiology. 1977;14:81–3.
4)

Ellis GL. Subdural haematoma in the elderly. Emerg Med Clin North Am. 1990;8:281–94.
5)

Karasawa H, Tomita S, Suzuki S. Chronic subdural haematomas: Time density curve and iodine concentrations in enhanced CT. Neuroradiology. 1987;29:36–9.
6)

Kim KS, Hemmati M, Weinberg P. Computed tomography in isodense subdural haematoma. Radiology. 1978;128:71–4.
7)

Fujisawa H, Nomura S, Kajiwara K, Kato S, Fujii M, Suzuki M. Various magnetic resonance imaging patterns of chronic subdural hematomas: indicators of the pathogenesis? Neurol Med Chir (Tokyo) 2006;46:333–9.
8)

Kelly AB, Zimmerman RD, Snow RB, Gandy SE, Heier LA, Deck MD. Head trauma: Comparison of MR and CT experience in 100 patients. AJNR Am J Neuroradiol. 1988;9:699–708.
9)

Guenot M. Chronic subdural haematoma: diagnostic imaging studies. Neurochirurgie. 2001;47:473–8.
10)

Hosoda K, Tamaki N, Masumura M, Matsumoto S, Maeda F. Magnetic resonance images of chronic subdural hematomas. J Neurosurg. 1987;67:677–83.
11)

Agrawal A. Bilateral biconvex frontal chronic subdural hematoma mimicking extradural hematoma. J Surg Tech Case Rep. 2010 Jul;2(2):90-1. doi: 10.4103/2006-8808.73625. PubMed PMID: 22091345; PubMed Central PMCID: PMC3214288.
12)

Sadrolhefazi A, Bloomfield SM. Interhemispheric and bilateral chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):455-63. Review. PubMed PMID: 10918015.
13) , 16)

Kurokawa Y, Ishizaki E, Inaba K. Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. Surg Neurol. 2005 Nov;64(5):444-9; discussion 449. PubMed PMID: 16253697.
14) , 18)

Andersen-Ranberg NC, Poulsen FR, Bergholt B, Hundsholt T, Fugleholm K. Bilateral chronic subdural hematoma: unilateral or bilateral drainage? J Neurosurg. 2017 Jun;126(6):1905-1911. doi: 10.3171/2016.4.JNS152642. Epub 2016 Jul 8. PubMed PMID: 27392267.
19)

Fujitani S, Ishikawa O, Miura K, Takeda Y, Goto H, Maeda K. Factors predicting contralateral hematoma growth after unilateral drainage of bilateral chronic subdural hematoma. J Neurosurg. 2017 Mar;126(3):755-759. doi: 10.3171/2016.1.JNS152655. PubMed PMID: 27081904.
21)

Chen L, Dong L, Wang XD, Zhang HZ, Wei M, She L. Bilateral Chronic Subdural Hematoma Treated by YL-1 Type Hematoma Aspiration Needle Complicated by Hemorrhage of the Basal Ganglia and Brainstem. World Neurosurg. 2017 Jan;97:761.e11-761.e13. doi: 10.1016/j.wneu.2016.09.074. PubMed PMID: 27702707.
22)

Siddiqui SA, Singh PK, Sawarkar D, Singh M, Sharma BS. Bilateral Ossified Chronic Subdural Hematoma Presenting as Diabetes Insipidus-Case Report and Literature Review. World Neurosurg. 2017 Feb;98:520-524. doi: 10.1016/j.wneu.2016.11.031. Review. PubMed PMID: 27867130.
23)

Suman S, Meenakshisundaram S, Woodhouse P. Bilateral chronic subdural haematoma: a reversible cause of parkinsonism. J R Soc Med. 2006 Feb;99(2):91-2. PubMed PMID: 16449784; PubMed Central PMCID: PMC1360497.

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)
By Christopher Yeoh

A Different Perspective After Brain Injury: A Tilted Point of View (After Brain Injury: Survivor Stories)

List Price: $170.00

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Whilst preparing for his travel adventures into a world he had yet to explore, Christopher Yeoh was involved in a road traffic accident and experienced something few others would be “privileged” to witness. Eight days in a coma, more than a year in and out of hospital and a gradual re-introduction to the world of work.

A Different Perspective After Brain Injury: A Tilted Point of View is written entirely by the survivor, providing an unusually introspective and critical personal account of life following a serious blow to the head. It charts the initial insult, early rehabilitation, development of understanding, the return of emotion, moments of triumph and regression into depression, the exercise of reframing how a brain injury is perceived and a return to work. It also describes the mental adjustments of awareness and acceptance alongside the physical recovery process.

Readily accessible to the general public, this book will also be of particular interest to professionals involved in the care of people who have had significant brain injuries, brain injury survivors, their families and friends and also those who fund and organise health and social care. This unique author account will provide a degree of understanding of what living with a hidden disability is really like.


Product Details

  • Published on: 2017-06-20
  • Original language: English
  • Binding: Hardcover
  • 154 pages

Editorial Reviews

Review

‘This very engaging book, written by a high functioning survivor of a traumatic brain injury, gives an introspective and critical account of what it actually feels like to suffer a brain injury and ‘come through the other side’. Christopher Yeoh integrates his phenomenological experience of brain injury with science, literature, autobiography, and philosophy, resulting in an extremely readable account of his experience. It provides a real ‘insider’s view’ of brain injury not possible to capture in a purely academic textbook. For this reason, the book will be of huge importance not only to the individuals and their families affected by brain injury, but also the clinicians involved in their care and rehabilitation.’ Rudi Coetzer, Consultant Neuropsychologist, North Wales Brain Injury Service, Betsi Cadwaladr UHB NHS Wales and Senior Lecturer in Clinical Neuropsychology, School of Psychology, Bangor University.

‘Christopher’s poignant narrative of his recovery and rehabilitation shows how personal characteristics and social resources interact to overcome the serious aftermath of severe traumatic brain injury. This is a balanced and insightful account of loss, challenge and triumph. He writes with humility and humour, whilst never masking the devastation the injury caused for him and his loved ones. Many inspiring books are written by survivors; A Different Perspective After Brain Injury will strike a chord with people grappling with changes to self in the context of ANY major life change. This is also an invaluable resource for clinicians, researchers and educators who seek a deeper understanding of the experience of brain injury.’ – Professor Tamara Ownsworth, School of Applied Psychology, Griffith University, Australia

About the Author

Christopher Yeoh is a holder of an LLB and LLM from the London School of Economics. He continues to practice securities law as a solicitor of England and Wales at a major global law firm.

After his adventure he now runs a multi award winning food and travel blog at quieteating.com and is a featured photographer in the Telegraph and Sunday Times newspapers. His photos have also been featured in brochures by the luxury travel company, Audley Travel.

As an action man he was previously an avid triathlete and a national award winning karateka. Now he prefers a slower pace of life by writing and irritating people with his camera.

Life after brain injury is not something less but just something different.

Book: Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)

Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)
By Blessen C Eapen MD, David X. Cifu MD

Traumatic Brain Injury Rehabilitation, An Issue of Physical Medicine and Rehabilitation Clinics of North America, 1e (The Clinics: Orthopedics)

List Price:$98.99

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This issue will focus on traumatic brain injury and will include articles on the following: Pathophysiology of TBI; Acute Management of Moderate-Severe TBI; Disorder of Consciousness; Rehabilitation of Moderate-Severe TBI; Acute Diagnosis and Management of Concussion; Rehabilitation of Persistent Symptoms after Concussion Chronic Traumatic Encephalopathy; Unique Aspect of TBI in the Military and Veteran; and many more!


Product Details

  • Published on: 2017-05-31
  • Original language: English
  • Dimensions: 8.27″ h x .87″ w x 5.91″ l,
  • Binding: Hardcover